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  • Mice, Inbred C57BL  (324)
  • American Association for the Advancement of Science (AAAS)  (324)
  • American Geophysical Union (AGU)
  • American Physical Society
  • Public Library of Science
  • 2015-2019  (50)
  • 2010-2014  (207)
  • 1990-1994  (67)
  • 1945-1949
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (324)
  • American Geophysical Union (AGU)
  • American Physical Society
  • Public Library of Science
  • Nature Publishing Group (NPG)  (365)
Years
Year
  • 1
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    Presentation of exogenous antigen with class I major histocompatibility complex molecules (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: Soluble antigens (Ags) in the extracellular fluids are excluded from the class I major histocompatibility complex (MHC)-restricted pathway of Ag presentation in most cells. However, an exogenous Ag can be internalized, processed, and presented in association with class I MHC molecules on specialized Ag-presenting cells (APCs). These APCs express class II molecules and can simultaneously present exogenous Ags to both class I and class II MHC-restricted T cells. These APCs may be important participants in the regulation of host immune responses. This APC activity may explain several phenomena of cytotoxic T lymphocyte (CTL) priming in vivo and might be exploited for eliciting CTL responses to protein vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, K L -- Gamble, S -- Rothstein, L -- AI-20248/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Azides/pharmacology ; Cell Line ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Inbred C57BL ; Ovalbumin/*immunology ; Spleen/immunology ; T-Lymphocytes/drug effects/immunology ; T-Lymphocytes, Cytotoxic/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: Primary and secondary hypertriglyceridemia is common in the general population, but the biochemical basis for this disease is largely unknown. With the use of transgenic technology, two lines of mice were created that express the human apolipoprotein CIII gene. One of these mouse lines with 100 copies of the gene was found to express large amounts of the protein and to be severely hypertriglyceridemic. The other mouse line with one to two copies of the gene expressed low amounts of the protein, but nevertheless manifested mild hypertriglyceridemia. Thus, overexpression of apolipoprotein CIII can be a primary cause of hypertriglyceridemia in vivo and may provide one possible etiology for this common disorder in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Y -- Azrolan, N -- O'Connell, A -- Walsh, A -- Breslow, J L -- HL 36461/HL/NHLBI NIH HHS/ -- HL33435/HL/NHLBI NIH HHS/ -- HL33714/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):790-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2167514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins C/blood/*genetics ; Chylomicrons/blood ; Cloning, Molecular ; DNA Restriction Enzymes/metabolism ; DNA, Recombinant/metabolism ; *Gene Expression ; Humans ; Hypertriglyceridemia/blood/*genetics ; Lipoproteins, VLDL/blood ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Triglycerides/blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    A mouse model of the aniridia-Wilms tumor deletion syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation. An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome. Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia. Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man. Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas. These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation. A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, T -- Lane, J -- Housman, D -- 2 T32 GMO7753-11/GM/NIGMS NIH HHS/ -- GM27882/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):823-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aniridia/*genetics ; Blotting, Southern ; Chromosome Deletion ; Chromosome Mapping ; DNA/analysis ; *Disease Models, Animal ; Eye/embryology/pathology ; Female ; Genes, Wilms Tumor/*genetics ; Genetic Markers ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muridae ; Mutation ; Phenotype ; Polymorphism, Genetic ; Syndrome ; Wilms Tumor/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Thymic epithelium tolerizes for histocompatibility antigens (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: The role of thymic epithelium in the establishment of tissue tolerance was analyzed with a murine chimeric system. All T cells differentiated from birth onward in a thymus comprising allogeneic epithelium and syngeneic hematopoietic cells. Embryonic thymic rudiments that contained no hematopoietic cells from C3H (H-2k) donors were grafted to newborn athymic (nude) BALB/c (H-2d) mice. Chimeras that had normal T cell numbers and function rejected third-party skin grafts, but permanently accepted grafts syngeneic to the thymic epithelium. In vitro functional assays did not always correlate with the state of tolerance in vivo. Thus, pure thymic epithelium induces tolerance to histocompatibility antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salaun, J -- Bandeira, A -- Khazaal, I -- Calman, F -- Coltey, M -- Coutinho, A -- Le Douarin, N M -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instit d'Embryologie cellulaire et moleculaire du CNRS, College de France, Nogent-sur-Marne.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; Epithelium/immunology ; Graft Rejection/immunology ; Graft Survival/*immunology ; Histocompatibility Antigens/*immunology ; Immune Tolerance/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Nude ; Thymus Gland/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Subtle cerebellar phenotype in mice homozygous for a targeted deletion of the En-2 homeobox (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: The two mouse genes, En-1 and En-2, that are homologs of the Drosophila segmentation gene engrailed, show overlapping spatially restricted patterns of expression in the neural tube during embryogenesis, suggestive of a role in regional specification. Mice homozygous for a targeted mutation that deletes the homeobox were viable and showed no obvious defects in embryonic development. This may be due to functional redundancy of En-2 and the related En-1 gene product during embryogenesis. Consistent with this hypothesis, the mutant mice showed abnormal foliation in the adult cerebellum, where En-2, and not En-1, is normally expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joyner, A L -- Herrup, K -- Auerbach, B A -- Davis, C A -- Rossant, J -- HD25334/HD/NICHD NIH HHS/ -- NS18381/NS/NINDS NIH HHS/ -- NS20591/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1239-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst ; Cell Line ; Cerebellum/*anatomy & histology/embryology/pathology ; Chimera ; *Chromosome Deletion ; Female ; *Genes, Homeobox ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nervous System/embryology ; Phenotype
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Direct molecular identification of the mouse pink-eyed unstable mutation by genome scanning (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: DNA sequences associated with the mouse pink-eyed unstable mutation were identified in the absence of closely linked molecular markers and without prior knowledge of the encoded gene product. This was accomplished by "genome scanning," a technique in which high-resolution Southern blots of genomic DNAs were hybridized to a dispersed and moderately repetitive DNA sequence. In this assay, pink-eyed unstable DNA was distinguished from the DNA of wild-type and revertant mice by enhanced hybridization to one of several hundred resolved fragments. The fragment showing enhanced hybridization in pink-eyed unstable DNA was cloned and found to lie within a DNA duplication that is located close to, or within, the pink-eyed dilution locus. The duplication associated with the mouse pink-eyed unstable mutation may mediate the high reversion frequency characteristic of this mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brilliant, M H -- Gondo, Y -- Eicher, E M -- CA06927/CA/NCI NIH HHS/ -- GM43840/GM/NIGMS NIH HHS/ -- RR05529/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1673574" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Blotting, Southern/methods ; DNA/genetics/isolation & purification ; Eye Color/*genetics ; *Genes ; Homozygote ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Restriction Mapping ; Tyrosine 3-Monooxygenase/genetics
    Print ISSN: 0036-8075
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  • 7
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    Linkage of faulty major histocompatibility complex class I to autoimmune diabetes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Pancreatic islet cells are the targets of an autoimmune response in type I diabetes. In the nonobese diabetic (NOD) mouse model of autoimmune diabetes, expression of major histocompatibility complex (MHC) class I proteins was inversely correlated with diabetes; in this mouse a mutation in the MHC class II-linked gene for the putative MHC class I peptide transporter was also present. Mice deficient in MHC class I expression because they do not produce beta 2-microglobulin also developed late onset autoimmune diabetes. In cells from humans with type I diabetes expression of MHC class I was decreased; subsets of prediabetics categorized as most likely to become hyperglycemic also had low MHC class I. T cell responses to self antigens are faulty in diabetics. In sets of genetically identical twins that are discordant for diabetes, the defect appeared to reside with the antigen presenting cell. Thus, a lack of surface MHC class I protein is associated with autoimmune diabetes; the concomitant defect in antigen presentation may impair the development of self tolerance, which could result in autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faustman, D -- Li, X P -- Lin, H Y -- Fu, Y E -- Eisenbarth, G -- Avruch, J -- Guo, J -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1756-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Cytotoxicity, Immunologic ; Diabetes Mellitus, Type 1/genetics/*immunology ; Diseases in Twins ; Flow Cytometry ; Gene Expression ; *Genes, MHC Class I ; Humans ; *Lymphocyte Activation ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Prediabetic State/genetics/immunology ; Spleen/immunology ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
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  • 8
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    Maintenance of normoglycemia in diabetic mice by subcutaneous xenografts of encapsulated islets (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: The goal of islet transplantation in human diabetes is to maintain the islet grafts in the recipients without the use of immunosuppression. One approach is to encapsulate the donor islets in permselective membranes. Hollow fibers fabricated from an acrylic copolymer were used to encapsulate small numbers of rat islets that were immobilized in an alginate hydrogel for transplantation in diabetic mice. The fibers were biocompatible, prevented rejection, and maintained normoglycemia when transplanted intraperitoneally; hyperglycemia returned when the fibers were removed at 60 days. Normoglycemia was also maintained by subcutaneous implants that had an appropriately constructed outer surface on the fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacy, P E -- Hegre, O D -- Gerasimidi-Vazeou, A -- Gentile, F T -- Dionne, K E -- DK01226/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763328" target="_blank"〉PubMed〈/a〉
    Keywords: *Acrylic Resins ; Animals ; Animals, Newborn ; Blood Glucose/*metabolism ; Diabetes Mellitus, Experimental/blood/*surgery ; In Vitro Techniques ; Insulin/secretion ; Islets of Langerhans/*secretion ; Islets of Langerhans Transplantation/*physiology ; Male ; Membranes, Artificial ; Mice ; Mice, Inbred C57BL ; *Polyvinyl Chloride ; Rats ; Rats, Inbred WF ; Time Factors ; Transplantation, Heterologous
    Print ISSN: 0036-8075
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  • 9
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    Tolerance in transgenic mice expressing major histocompatibility molecules extrathymically on pancreatic cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: Transgenic mice with defined expression of major histocompatibility complex (MHC) proteins provide novel systems for understanding the fundamental question of T cell tolerance to nonlymphoid self components. The MHC class II I-E and I-A and class I H-2K molecules expressed specifically on pancreatic islet or acinar cells serve as model self antigens. In these systems, transgenic proteins are not detected in the thymus or other lymphoid tissues. Yet mice are tolerant to the pancreatic MHC products in vivo; this tolerance is not induced by clonal deletion. These studies have been aided by monoclonal antibodies specific for I-E-reactive T cells and indicate that clonal anergy may be an important mechanism of tolerance to peripheral proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burkly, L C -- Lo, D -- Flavell, R A -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1364-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen Incorporated, 14 Cambridge Center, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Autoantigens/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; Islets of Langerhans/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Generation and analysis of interleukin-4 deficient mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: Interleukin-4 (IL-4) promotes the growth and differentiation of many hematopoietic cells in vitro; in particular, it directs the immunoglobulin (Ig) class switch to IgG1 and IgE. Mice homozygous for a mutation that inactivates the IL-4 gene were generated to test the requirement for IL-4 in vivo. In the mutant mice T and B cell development was normal, but the serum levels of IgG1 and IgE were strongly reduced. The IgG1 dominance in a T cell-dependent immune response was lost, and IgE was not detectable upon nematode infection. Thus, some but not all of the in vitro properties of IL-4 are critical for the physiology of the immune system in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhn, R -- Rajewsky, K -- Muller, W -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948049" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Alleles ; Animals ; B-Lymphocytes/immunology ; Blotting, Southern ; Chromosome Deletion ; Concanavalin A ; DNA/genetics/isolation & purification ; Female ; Interleukin-4/deficiency/*genetics ; Lymph Nodes/growth & development/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Restriction Mapping ; Spleen/growth & development/immunology ; T-Lymphocytes/immunology ; Thymus Gland/growth & development/immunology
    Print ISSN: 0036-8075
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  • 11
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    Age-associated inclusions in normal and transgenic mouse brain (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, M -- Walker, L C -- Martin, L J -- Kitt, C A -- Kleinman, H K -- Ingram, D K -- Price, D L -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1443-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542796" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    An animal model for cystic fibrosis made by gene targeting (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Cystic fibrosis results from defects in the gene encoding a cyclic adenosine monophosphate-dependent chloride ion channel known as the cystic fibrosis transmembrane conductance regulator (CFTR). To create an animal model for cystic fibrosis, mice were generated from embryonic stem cells in which the CFTR gene was disrupted by gene targeting. Mice homozygous for the disrupted gene display many features common to young human cystic fibrosis patients, including failure to thrive, meconium ileus, alteration of mucous and serous glands, and obstruction of glandlike structures with inspissated eosinophilic material. Death resulting from intestinal obstruction usually occurs before 40 days of age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snouwaert, J N -- Brigman, K K -- Latour, A M -- Malouf, N N -- Boucher, R C -- Smithies, O -- Koller, B H -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1083-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27599-7020.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cystic Fibrosis/*genetics/pathology/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Digestive System/metabolism/pathology ; *Disease Models, Animal ; Exocrine Glands/pathology ; Gallbladder/pathology ; Genitalia, Male/pathology ; Genotype ; Growth ; Intestinal Obstruction/etiology/pathology ; Liver/pathology ; Male ; Meconium/metabolism ; Membrane Proteins/*genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mucus/metabolism ; Mutagenesis ; Pancreas/pathology ; RNA, Messenger/metabolism ; Salivary Glands/pathology
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  • 13
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    A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: In a pedigree derived from a mouse treated with the mutagen ethylnitrosourea, a mutation has been identified that predisposes to spontaneous intestinal cancer. The mutant gene was found to be dominantly expressed and fully penetrant. Affected mice developed multiple adenomas throughout the entire intestinal tract at an early age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, A R -- Pitot, H C -- Dove, W F -- CA07175/CA/NCI NIH HHS/ -- CA50585/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):322-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2296722" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/complications/*genetics ; Alleles ; Anemia/complications/genetics ; Animals ; Ethylnitrosourea ; Female ; Intestinal Neoplasms/complications/*genetics/pathology ; Male ; Mice ; Mice, Inbred AKR ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Shared actions of endotoxin and taxol on TNF receptors and TNF release (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Bacterial lipopolysaccharide (LPS) exerts profound effects on mammalian hosts in part by inducing macrophages to release tumor necrosis factor-alpha (TNF-alpha); the mechanisms involved are unresolved. The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-alpha receptors and triggered TNF-alpha release. Both actions of taxol were absent in LPS-hyporesponsive C3H/HeJ mice. In recombinant inbred mice, the genes controlling responses to LPS and to taxol were closely linked. Dexamethasone blocked release of TNF-alpha by both stimuli but did not block the decrease in TNF-alpha receptors. Thus, a protein associated with microtubules may be a cellular target of LPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, A H -- Porteu, F -- Sanchez, E -- Nathan, C F -- CA-43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1970196" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/*pharmacology ; Animals ; Crosses, Genetic ; Dexamethasone/pharmacology ; Lipopolysaccharides/*pharmacology ; Macrophages/*drug effects/metabolism ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Paclitaxel ; Receptors, Cell Surface/*drug effects/metabolism ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Inhibition of T cell receptor expression and function in immature CD4+CD8+ cells by CD4 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: Most immature CD4+CD8+ thymocytes express only a small number of T cell receptor (TCR) molecules on their surface, and the TCR molecules they do express are only marginally capable of transducing intracellular signals. TCR expression and function was not intrinsically low in immature CD4+CD8+ thymocytes, but was found to be actively inhibited by CD4-mediated signals. Indeed, release of CD4+CD8+ thymocytes from CD4-mediated signals resulted in significant increases in both TCR expression and signaling function. These results suggest that, in CD4+CD8+ cells developing in the thymus, increased TCR expression and function requires release from CD4-mediated inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, T -- June, C H -- Munitz, T I -- Sheard, M -- McCarthy, S A -- Sharrow, S O -- Samelson, L E -- Singer, A -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2120773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD4/*immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cell Membrane/immunology ; Cells, Cultured ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/biosynthesis/*physiology ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Regulation of alloreactivity in vivo by a soluble form of the interleukin-1 receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: In vitro studies have shown that cytokines are involved in the regulation of the immune response, but their role in vivo is less well defined. Specific cytokine antagonists enable the identification of particular cytokines involved in the response and offer a means for modifying it. Systemic administration of a soluble, extracellular portion of the receptor for interleukin-1 (sIL-1R) had profound inhibitory effects on the development of in vivo alloreactivity. Survival of heterotopic heart allografts was prolonged from 12 days in controls to 17 days in mice treated with sIL-1R. Lymph node hyperplasia in response to a localized injection of allogeneic cells was completely blocked by sIL-1R treatment. The inhibition was overcome by simultaneous administration of interleukin-1 (IL-1); thus, sIL-1R acts by neutralizing IL-1. These results implicate IL-1 as a regulator of allograft rejection and demonstrate the in vivo biological efficacy of a soluble cytokine receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fanslow, W C -- Sims, J E -- Sassenfeld, H -- Morrissey, P J -- Gillis, S -- Dower, S K -- Widmer, M B -- New York, N.Y. -- Science. 1990 May 11;248(4956):739-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2139736" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Graft Rejection ; *Graft Survival ; H-2 Antigens/immunology ; Heart Transplantation/*immunology ; Immunosuppression ; Interleukin-1/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/immunology ; Receptors, Immunologic/*immunology ; Receptors, Interleukin-1 ; Transplantation, Heterotopic ; Transplantation, Homologous
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Limit of T cell tolerance to self proteins by peptide presentation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: Cytotoxic T lymphocytes (CTLs) recognize foreign peptides bound to major histocompatibility complex (MHC) class I molecules. MHC molecules can also bind endogenous self peptides, to which T cells are tolerant. Normal mice contained CTLs specific for self peptides that were from proteins of ubiquitous or tissue-restricted expression. In vivo, these endogenous self peptides are not naturally presented in sufficient density by somatic cells expressing MHC class I molecules. They can, however, be presented if added exogenously. Thus, our data imply that CTLs are only tolerant of those endogenous self peptide sequences that are presented by MHC class I-positive cells in a physiological manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schild, H -- Rotzschke, O -- Kalbacher, H -- Rammensee, H G -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1587-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Biologie, Abteilung Immungenetik, Tubingen, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Cell Line ; Histocompatibility Antigens Class I/*immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred C57BL ; Peptide Fragments/*immunology ; T-Lymphocytes, Cytotoxic/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Depletion of CD4+ T cells in major histocompatibility complex class II-deficient mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-20
    Description: The maturation of T cells in the thymus is dependent on the expression of major histocompatibility complex (MHC) molecules. By disruption of the MHC class II Ab beta gene in embryonic stem cells, mice were generated that lack cell surface expression of class II molecules. These MHC class II-deficient mice were depleted of mature CD4+ T cells and were deficient in cell-mediated immune responses. These results provide genetic evidence that class II molecules are required for the maturation and function of mature CD4+ T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grusby, M J -- Johnson, R S -- Papaioannou, V E -- Glimcher, L H -- AI21569/AI/NIAID NIH HHS/ -- HD27295/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 20;253(5026):1417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1910207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*immunology ; Crosses, Genetic ; Embryo, Mammalian ; Enzyme-Linked Immunosorbent Assay ; Female ; *Genes, MHC Class II ; Immunity, Cellular/genetics ; Immunoglobulin G/analysis/classification ; Immunoglobulin M/analysis ; Immunologic Deficiency Syndromes/*genetics ; *Lymphocyte Depletion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Stem Cells/immunology ; T-Lymphocyte Subsets/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Induction of self-tolerance in T cells but not B cells of transgenic mice expressing little self antigen (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Self-tolerance to a transgene-encoded protein, hen egg lysozyme, was examined in the T and B cell repertoires of a series of lines of transgenic mice that expressed different serum concentrations of soluble lysozyme. T cells were tolerant in all lines in which lysozyme was expressed irrespective of the antigen concentration, whereas B cell tolerance did not occur when the serum lysozyme concentration was less than 1.5 nanograms per milliliter (0.1 nM). Induction of elevated transgene expression could restore B cell tolerance. These findings support the hypothesis that autoimmune disease may in some instances arise through a bypass of T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adelstein, S -- Pritchard-Briscoe, H -- Anderson, T A -- Crosbie, J -- Gammon, G -- Loblay, R H -- Basten, A -- Goodnow, C C -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1223-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Chickens ; Egg White ; Enzyme-Linked Immunosorbent Assay ; Female ; Fluorescein-5-isothiocyanate ; Fluoresceins ; Fluorescent Dyes ; *Immune Tolerance ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muramidase/blood/*genetics/immunology ; T-Lymphocytes/*immunology ; Thiocyanates
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Diet-induced hypercholesterolemia in mice: prevention by overexpression of LDL receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: The current studies were designed to determine whether chronic overexpression of low density lipoprotein (LDL) receptors in the liver would protect mice from the increase in plasma LDL-cholesterol that is induced by high-fat diets. A line of transgenic mice was studied that express the human LDL receptor gene in the liver under control of the transferrin promoter. When fed a diet containing cholesterol, saturated fat, and bile acids for 3 weeks, the transgenic mice, in contrast to normal mice, did not develop a detectable increase in plasma LDL. The current data indicate that unregulated overexpression of LDL receptors can protect against diet-induced hypercholesterolemia in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokode, M -- Hammer, R E -- Ishibashi, S -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1273-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol, Dietary/adverse effects ; Cholesterol, LDL/*blood ; Dietary Fats/*adverse effects ; Exons ; *Gene Expression ; Humans ; Hypercholesterolemia/etiology/*prevention & control ; Introns ; Lipoproteins/blood ; Lipoproteins, HDL/blood ; Lipoproteins, IDL ; Lipoproteins, VLDL/blood ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nucleic Acid Hybridization ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; Receptors, LDL/*genetics ; Transferrin/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; beta 2-microglobulin (beta 2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta 2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta 2M gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4- CD8+ T cells, which normally mediate cytotoxic T cell function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, B H -- Marrack, P -- Kappler, J W -- Smithies, O -- AI-18785/AI/NIAID NIH HHS/ -- GM20069/GM/NIGMS NIH HHS/ -- HL37001/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1227-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2112266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*genetics ; Chimera ; Gene Expression ; Genes ; Genes, MHC Class I ; Histocompatibility Antigens Class I/*genetics ; Lymph Nodes/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Spleen/immunology ; T-Lymphocytes/*immunology ; beta 2-Microglobulin/*deficiency/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    The role of B cells for in vivo T cell responses to a Friend virus-induced leukemia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: B cells can function as antigen-presenting cells and accessory cells for T cell responses. This study evaluated the role of B cells in the induction of protective T cell immunity to a Friend murine leukemia virus (F-MuLV)-induced leukemia (FBL). B cell-deficient mice exhibited significantly reduced tumor-specific CD4+ helper and CD8+ cytotoxic T cell responses after priming with FBL or a recombinant vaccinia virus containing F-MuLV antigens. Moreover, these mice had diminished T cell responses to the vaccinia viral antigens. Tumor-primed T cells transferred into B cell-deficient mice effectively eradicated disseminated FBL. Thus, B cells appear necessary for efficient priming but not expression of tumor and viral T cell immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schultz, K R -- Klarnet, J P -- Gieni, R S -- HayGlass, K T -- Greenberg, P D -- CA 33084/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2118273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD4/analysis ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; B-Lymphocytes/*immunology ; Friend murine leukemia virus/*immunology ; Genes, MHC Class I ; Immunization, Passive ; Leukemia, Experimental/*immunology/therapy ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccinia virus/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-01
    Description: Germ-line mutations of the APC gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominantly inherited disease in humans. Patients with FAP develop multiple benign colorectal tumors. Recently, a mouse lineage that exhibits an autosomal dominantly inherited predisposition to multiple intestinal neoplasia (Min) was described. Linkage analysis showed that the murine homolog of the APC gene (mApc) was tightly linked to the Min locus. Sequence comparison of mApc between normal and Min-affected mice identified a nonsense mutation, which cosegregated with the Min phenotype. This mutation is analogous to those found in FAP kindreds and in sporadic colorectal cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, L K -- Kinzler, K W -- Vogelstein, B -- Preisinger, A C -- Moser, A R -- Luongo, C -- Gould, K A -- Dove, W F -- CA-06973/CA/NCI NIH HHS/ -- CA-07175/CA/NCI NIH HHS/ -- CA-23076/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 May 1;256(5057):668-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1350108" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Animals ; Base Sequence ; Blotting, Southern ; Colorectal Neoplasms/genetics ; DNA, Neoplasm/chemistry/genetics ; *Genes, Tumor Suppressor ; Genetic Linkage ; Humans ; Intestinal Neoplasms/*genetics ; Mice ; Mice, Inbred AKR ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Mutation ; Phenotype ; Polymorphism, Restriction Fragment Length ; Sequence Homology, Nucleic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Activation-induced ubiquitination of the T cell antigen receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: The zeta subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta molecules were modified, and at least one other TCR subunit, CD3 delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cenciarelli, C -- Hou, D -- Hsu, K C -- Rellahan, B L -- Wiest, D L -- Smith, H T -- Fried, V A -- Weissman, A M -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology/metabolism ; Cells, Cultured ; Hybridomas/immunology ; Lymphocyte Activation/*physiology ; Macromolecular Substances ; Mice ; Mice, Inbred C57BL ; Molecular Weight ; *Protein Processing, Post-Translational ; Receptors, Antigen, T-Cell/immunology/isolation & purification/*metabolism ; Spleen/immunology ; T-Lymphocytes/*immunology ; Ubiquitins/isolation & purification/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 25
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    PRDM9 is a major determinant of meiotic recombination hotspots in humans and mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Meiotic recombination events cluster into narrow segments of the genome, defined as hotspots. Here, we demonstrate that a major player for hotspot specification is the Prdm9 gene. First, two mouse strains that differ in hotspot usage are polymorphic for the zinc finger DNA binding array of PRDM9. Second, the human consensus PRDM9 allele is predicted to recognize the 13-mer motif enriched at human hotspots; this DNA binding specificity is verified by in vitro studies. Third, allelic variants of PRDM9 zinc fingers are significantly associated with variability in genome-wide hotspot usage among humans. Our results provide a molecular basis for the distribution of meiotic recombination in mammals, in which the binding of PRDM9 to specific DNA sequences targets the initiation of recombination at specific locations in the genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295902/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295902/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baudat, F -- Buard, J -- Grey, C -- Fledel-Alon, A -- Ober, C -- Przeworski, M -- Coop, G -- de Massy, B -- 03S1/PHS HHS/ -- GM83098/GM/NIGMS NIH HHS/ -- HD21244/HD/NICHD NIH HHS/ -- HL085197/HL/NHLBI NIH HHS/ -- R01 GM083098/GM/NIGMS NIH HHS/ -- R01 HD021244/HD/NICHD NIH HHS/ -- R01 HL085197/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):836-40. doi: 10.1126/science.1183439. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique Humaine, UPR1142, CNRS, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044539" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/chemistry/metabolism ; DNA Breaks, Double-Stranded ; DNA-Binding Proteins/chemistry/genetics/metabolism ; Genome ; Genome, Human ; Genotype ; Histone-Lysine N-Methyltransferase/chemistry/*genetics/*metabolism ; Humans ; Meiosis/*genetics ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Phenotype ; *Recombination, Genetic ; Zinc Fingers/genetics
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    The ligase PIAS1 restricts natural regulatory T cell differentiation by epigenetic repression (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: CD4(+)Foxp3(+) regulatory T (T(reg)) cells are important for maintaining immune tolerance. Understanding the molecular mechanism that regulates T(reg) differentiation will facilitate the development of effective therapeutic strategies against autoimmune diseases. We report here that the SUMO E3 ligase PIAS1 restricts the differentiation of natural T(reg) cells by maintaining a repressive chromatin state of the Foxp3 promoter. PIAS1 acts by binding to the Foxp3 promoter to recruit DNA methyltransferases and heterochromatin protein 1 for epigenetic modifications. Pias1 deletion caused promoter demethylation, reduced histone H3 methylation at Lys(9), and enhanced promoter accessibility. Consistently, Pias1(-/-) mice displayed an increased natural T(reg) cell population and were resistant to the development of experimental autoimmune encephalomyelitis. Our studies have identified an epigenetic mechanism that negatively regulates the differentiation of natural T(reg) cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3043201/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3043201/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Bin -- Tahk, Samuel -- Yee, Kathleen M -- Fan, Guoping -- Shuai, Ke -- K01 AR52717-01/AR/NIAMS NIH HHS/ -- R01 AI063286/AI/NIAID NIH HHS/ -- R01 AI063286-05/AI/NIAID NIH HHS/ -- R01 GM085797/GM/NIGMS NIH HHS/ -- R01 GM085797-03/GM/NIGMS NIH HHS/ -- R01AI063286/AI/NIAID NIH HHS/ -- R01GM085797/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):521-5. doi: 10.1126/science.1193787.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology-Oncology, Department of Medicine, 11-934 Factor Building, 10833 Le Conte Avenue, University of California, Los Angeles, Los Angeles, CA 90095, USA. bliu@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; CD4-Positive T-Lymphocytes/cytology ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/metabolism ; DNA Methylation ; Encephalomyelitis, Autoimmune, Experimental/immunology ; *Epigenesis, Genetic ; Female ; Forkhead Transcription Factors/genetics ; Histones/metabolism ; Lymphopoiesis/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Promoter Regions, Genetic ; Protein Inhibitors of Activated STAT/*physiology ; Repressor Proteins/*physiology ; T-Lymphocytes, Regulatory/*cytology/immunology ; Ubiquitin-Protein Ligases/*physiology
    Print ISSN: 0036-8075
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    Identification of RACK1 and protein kinase Calpha as integral components of the mammalian circadian clock (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: At the core of the mammalian circadian clock is a negative feedback loop in which the dimeric transcription factor CLOCK-BMAL1 drives processes that in turn suppress its transcriptional activity. To gain insight into the mechanisms of circadian feedback, we analyzed mouse protein complexes containing BMAL1. Receptor for activated C kinase-1 (RACK1) and protein kinase C-alpha (PKCalpha) were recruited in a circadian manner into a nuclear BMAL1 complex during the negative feedback phase of the cycle. Overexpression of RACK1 and PKCalpha suppressed CLOCK-BMAL1 transcriptional activity, and RACK1 stimulated phosphorylation of BMAL1 by PKCalpha in vitro. Depletion of endogenous RACK1 or PKCalpha from fibroblasts shortened the circadian period, demonstrating that both molecules function in the clock oscillatory mechanism. Thus, the classical PKC signaling pathway is not limited to relaying external stimuli but is rhythmically activated by internal processes, forming an integral part of the circadian feedback loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robles, Maria S -- Boyault, Cyril -- Knutti, Darko -- Padmanabhan, Kiran -- Weitz, Charles J -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):463-6. doi: 10.1126/science.1180067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093473" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Feedback, Physiological ; Fibroblasts/metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Neuropeptides/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinase C-alpha/*metabolism ; RNA Interference ; Signal Transduction ; Transcription, Genetic
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    Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-26
    Description: Ghrelin is a gastric peptide hormone that stimulates weight gain in vertebrates. The biological activities of ghrelin require octanoylation of the peptide on Ser(3), an unusual posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). Here, we describe the design, synthesis, and characterization of GO-CoA-Tat, a peptide-based bisubstrate analog that antagonizes GOAT. GO-CoA-Tat potently inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-CoA-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin-deficient mice, supporting the concept that its beneficial metabolic effects are due specifically to GOAT inhibition. In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, Brad P -- Hwang, Yousang -- Taylor, Martin S -- Kirchner, Henriette -- Pfluger, Paul T -- Bernard, Vincent -- Lin, Yu-yi -- Bowers, Erin M -- Mukherjee, Chandrani -- Song, Woo-Jin -- Longo, Patti A -- Leahy, Daniel J -- Hussain, Mehboob A -- Tschop, Matthias H -- Boeke, Jef D -- Cole, Philip A -- P01 CA016519/CA/NCI NIH HHS/ -- P01 CA016519-35/CA/NCI NIH HHS/ -- P30 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637-05/DK/NIDDK NIH HHS/ -- R01 DK081472/DK/NIDDK NIH HHS/ -- R01 DK081472-01A1/DK/NIDDK NIH HHS/ -- R01 DK081472-02/DK/NIDDK NIH HHS/ -- R01 DK081472-03/DK/NIDDK NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-04/GM/NIGMS NIH HHS/ -- R01 GM062437-11/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1689-92. doi: 10.1126/science.1196154. Epub 2010 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21097901" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Acyltransferases/*antagonists & inhibitors ; Animals ; Cell Survival/drug effects ; Drug Design ; Enzyme Inhibitors/chemical synthesis/*pharmacology/toxicity ; Ghrelin/deficiency/genetics/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; HeLa Cells ; Homeostasis ; Humans ; Insulin/metabolism ; Ion Channels/metabolism ; Islets of Langerhans/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Peptides/chemical synthesis/*pharmacology/toxicity ; Weight Gain/*drug effects
    Print ISSN: 0036-8075
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-02
    Description: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
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    Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manicassamy, Santhakumar -- Reizis, Boris -- Ravindran, Rajesh -- Nakaya, Helder -- Salazar-Gonzalez, Rosa Maria -- Wang, Yi-Chong -- Pulendran, Bali -- HHSN266 200700006C/PHS HHS/ -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI056499/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01DK057665,/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638,/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266,/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):849-53. doi: 10.1126/science.1188510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Dendritic Cells/*immunology/metabolism ; Gene Expression Profiling ; *Inflammation ; Inflammatory Bowel Diseases/*immunology ; Intestinal Mucosa/cytology/*immunology/metabolism ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Tretinoin/metabolism ; Wnt Proteins/metabolism ; beta Catenin/*metabolism
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    Cyclooxygenase-2 controls energy homeostasis in mice by de novo recruitment of brown adipocytes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: Obesity results from chronic energy surplus and excess lipid storage in white adipose tissue (WAT). In contrast, brown adipose tissue (BAT) efficiently burns lipids through adaptive thermogenesis. Studying mouse models, we show that cyclooxygenase (COX)-2, a rate-limiting enzyme in prostaglandin (PG) synthesis, is a downstream effector of beta-adrenergic signaling in WAT and is required for the induction of BAT in WAT depots. PG shifted the differentiation of defined mesenchymal progenitors toward a brown adipocyte phenotype. Overexpression of COX-2 in WAT induced de novo BAT recruitment in WAT, increased systemic energy expenditure, and protected mice against high-fat diet-induced obesity. Thus, COX-2 appears integral to de novo BAT recruitment, which suggests that the PG pathway regulates systemic energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vegiopoulos, Alexandros -- Muller-Decker, Karin -- Strzoda, Daniela -- Schmitt, Iris -- Chichelnitskiy, Evgeny -- Ostertag, Anke -- Berriel Diaz, Mauricio -- Rozman, Jan -- Hrabe de Angelis, Martin -- Nusing, Rolf M -- Meyer, Carola W -- Wahli, Walter -- Klingenspor, Martin -- Herzig, Stephan -- New York, N.Y. -- Science. 2010 May 28;328(5982):1158-61. doi: 10.1126/science.1186034. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emmy Noether and Marie Curie Research Group Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448152" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, Brown/cytology/*physiology ; Adipogenesis ; Adipose Tissue ; Adipose Tissue, Brown/cytology/*physiology ; Adipose Tissue, White/enzymology/*physiology ; Adrenergic beta-3 Receptor Agonists ; Adrenergic beta-Agonists/pharmacology ; Animals ; Body Weight ; Cyclooxygenase 2/*genetics/*metabolism ; Dietary Fats/administration & dosage ; Dioxoles/pharmacology ; *Energy Metabolism ; Female ; Gene Expression Regulation, Enzymologic ; Homeostasis ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mice, Transgenic ; Norepinephrine/metabolism ; Obesity/etiology/prevention & control ; Oxygen Consumption ; Prostaglandins/*metabolism ; Receptors, Adrenergic, beta-3/metabolism ; Signal Transduction ; *Thermogenesis
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    G protein subunit Galpha13 binds to integrin alphaIIbbeta3 and mediates integrin "outside-in" signaling (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-16
    Description: Integrins mediate cell adhesion to the extracellular matrix and transmit signals within the cell that stimulate cell spreading, retraction, migration, and proliferation. The mechanism of integrin outside-in signaling has been unclear. We found that the heterotrimeric guanine nucleotide-binding protein (G protein) Galpha13 directly bound to the integrin beta3 cytoplasmic domain and that Galpha13-integrin interaction was promoted by ligand binding to the integrin alphaIIbbeta3 and by guanosine triphosphate (GTP) loading of Galpha13. Interference of Galpha13 expression or a myristoylated fragment of Galpha13 that inhibited interaction of alphaIIbbeta3 with Galpha13 diminished activation of protein kinase c-Src and stimulated the small guanosine triphosphatase RhoA, consequently inhibiting cell spreading and accelerating cell retraction. We conclude that integrins are noncanonical Galpha13-coupled receptors that provide a mechanism for dynamic regulation of RhoA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842917/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Haixia -- Shen, Bo -- Flevaris, Panagiotis -- Chow, Christina -- Lam, Stephen C-T -- Voyno-Yasenetskaya, Tatyana A -- Kozasa, Tohru -- Du, Xiaoping -- GM061454/GM/NIGMS NIH HHS/ -- GM074001/GM/NIGMS NIH HHS/ -- HL062350/HL/NHLBI NIH HHS/ -- HL068819/HL/NHLBI NIH HHS/ -- HL080264/HL/NHLBI NIH HHS/ -- R01 GM061454/GM/NIGMS NIH HHS/ -- R01 GM061454-09/GM/NIGMS NIH HHS/ -- R01 GM074001/GM/NIGMS NIH HHS/ -- R01 GM074001-02/GM/NIGMS NIH HHS/ -- R01 HL062350/HL/NHLBI NIH HHS/ -- R01 HL062350-09/HL/NHLBI NIH HHS/ -- R01 HL068819/HL/NHLBI NIH HHS/ -- R01 HL068819-08/HL/NHLBI NIH HHS/ -- R01 HL080264/HL/NHLBI NIH HHS/ -- R01 HL080264-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):340-3. doi: 10.1126/science.1174779.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Illinois at Chicago, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Blood Platelets/*physiology ; Clot Retraction ; Fibrinogen/metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/genetics/*metabolism ; Humans ; Integrin beta3/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Platelet Adhesiveness ; Platelet Glycoprotein GPIIb-IIIa Complex/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; rhoA GTP-Binding Protein/antagonists & inhibitors/metabolism
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    Mcl-1 is essential for germinal center formation and B cell memory (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Lymphocyte survival during immune responses is controlled by the relative expression of pro- and anti-apoptotic molecules, regulating the magnitude, quality, and duration of the response. We investigated the consequences of deleting genes encoding the anti-apoptotic molecules Mcl1 and Bcl2l1 (Bcl-x(L)) from B cells using an inducible system synchronized with expression of activation-induced cytidine deaminase (Aicda) after immunization. This revealed Mcl1 and not Bcl2l1 to be indispensable for the formation and persistence of germinal centers (GCs). Limiting Mcl1 expression reduced the magnitude of the GC response with an equivalent, but not greater, effect on memory B cell formation and no effect on persistence. Our results identify Mcl1 as the main anti-apoptotic regulator of activated B cell survival and suggest distinct mechanisms controlling survival of GC and memory B cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991396/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vikstrom, Ingela -- Carotta, Sebastian -- Luthje, Katja -- Peperzak, Victor -- Jost, Philipp J -- Glaser, Stefan -- Busslinger, Meinrad -- Bouillet, Philippe -- Strasser, Andreas -- Nutt, Stephen L -- Tarlinton, David M -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1095-9. doi: 10.1126/science.1191793. Epub 2010 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; B-Lymphocytes/*immunology ; Cell Survival ; Gene Deletion ; Germinal Center/cytology/*immunology ; *Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2/genetics/*immunology ; bcl-X Protein/genetics/immunology
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    Prdm9 controls activation of mammalian recombination hotspots (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Mammalian meiotic recombination, which preferentially occurs at specialized sites called hotspots, ensures the orderly segregation of meiotic chromosomes and creates genetic variation among offspring. A locus on mouse chromosome 17, which controls activation of recombination at multiple distant hotspots, has been mapped within a 181-kilobase interval, three of whose genes can be eliminated as candidates. The remaining gene, Prdm9, codes for a zinc finger containing histone H3K4 trimethylase that is expressed in early meiosis and whose deficiency results in sterility in both sexes. Mus musculus exhibits five alleles of Prdm9; human populations exhibit two predominant alleles and multiple minor alleles. The identification of Prdm9 as a protein regulating mammalian recombination hotspots initiates molecular studies of this important biological control system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821451/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821451/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parvanov, Emil D -- Petkov, Petko M -- Paigen, Kenneth -- 076468/PHS HHS/ -- 078452/PHS HHS/ -- 083408/PHS HHS/ -- CA 34196/CA/NCI NIH HHS/ -- GM 078643/GM/NIGMS NIH HHS/ -- P30 CA034196-26/CA/NCI NIH HHS/ -- P50 GM076468/GM/NIGMS NIH HHS/ -- P50 GM076468-030004/GM/NIGMS NIH HHS/ -- R01 GM078452/GM/NIGMS NIH HHS/ -- R01 GM078452-02/GM/NIGMS NIH HHS/ -- R01 GM078643/GM/NIGMS NIH HHS/ -- R01 GM078643-03/GM/NIGMS NIH HHS/ -- R01 GM083408/GM/NIGMS NIH HHS/ -- R01 GM083408-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):835. doi: 10.1126/science.1181495. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044538" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Chromosome Mapping ; Female ; Histone-Lysine N-Methyltransferase/chemistry/*genetics/metabolism ; Humans ; Male ; Meiosis/*genetics ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Recombination, Genetic ; Sequence Analysis, DNA ; Testis/metabolism ; Zinc Fingers
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    Sex-specific parent-of-origin allelic expression in the mouse brain (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Genomic imprinting results in preferential gene expression from paternally versus maternally inherited chromosomes. We used a genome-wide approach to uncover sex-specific parent-of-origin allelic effects in the adult mouse brain. Our study identified preferential selection of the maternally inherited X chromosome in glutamatergic neurons of the female cortex. Moreover, analysis of the cortex and hypothalamus identified 347 autosomal genes with sex-specific imprinting features. In the hypothalamus, sex-specific imprinted genes were mostly found in females, which suggests parental influence over the hypothalamic function of daughters. We show that interleukin-18, a gene linked to diseases with sex-specific prevalence, is subject to complex, regional, and sex-specific parental effects in the brain. Parent-of-origin effects thus provide new avenues for investigation of sexual dimorphism in brain function and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997643/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- Zhang, Jiangwen -- Butler, James E -- Haig, David -- Dulac, Catherine -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):682-5. doi: 10.1126/science.1190831. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616234" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Crosses, Genetic ; Dioxygenases ; *Epigenesis, Genetic ; Female ; Gene Expression Profiling ; *Genes, X-Linked ; *Genomic Imprinting ; Glutamic Acid/metabolism ; Interleukin-18/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Neurons/metabolism ; Oxygenases/genetics ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/cytology/*metabolism ; Preoptic Area/cytology/*metabolism ; Ribosomal Proteins/genetics ; *Sex Characteristics ; Succinate Dehydrogenase/genetics ; X Chromosome Inactivation
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    Eppendorf winner. Parental control over the brain (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):770-1. doi: 10.1126/science.1199054.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. cgregg@MCB.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051625" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Awards and Prizes ; *Fathers ; *Gene Expression ; Gene Expression Profiling ; *Genomic Imprinting ; Humans ; Interleukin-18 ; Mice ; Mice, Inbred C57BL ; *Mothers ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/embryology/growth & development/*metabolism ; Preoptic Area/embryology/growth & development/*metabolism ; Sex Characteristics
    Print ISSN: 0036-8075
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    Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: Stem cells that naturally reside in adult tissues, such as muscle stem cells (MuSCs), exhibit robust regenerative capacity in vivo that is rapidly lost in culture. Using a bioengineered substrate to recapitulate key biophysical and biochemical niche features in conjunction with a highly automated single-cell tracking algorithm, we show that substrate elasticity is a potent regulator of MuSC fate in culture. Unlike MuSCs on rigid plastic dishes (approximately 10(6) kilopascals), MuSCs cultured on soft hydrogel substrates that mimic the elasticity of muscle (12 kilopascals) self-renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into mice and assayed histologically and quantitatively by noninvasive bioluminescence imaging. Our studies provide novel evidence that by recapitulating physiological tissue rigidity, propagation of adult muscle stem cells is possible, enabling future cell-based therapies for muscle-wasting diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, P M -- Havenstrite, K L -- Magnusson, K E G -- Sacco, A -- Leonardi, N A -- Kraft, P -- Nguyen, N K -- Thrun, S -- Lutolf, M P -- Blau, H M -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- 52005886/Howard Hughes Medical Institute/ -- AG009521/AG/NIA NIH HHS/ -- AG020961/AG/NIA NIH HHS/ -- CA09151/CA/NCI NIH HHS/ -- HL096113/HL/NHLBI NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG020961/AG/NIA NIH HHS/ -- R01 AG020961-06A2/AG/NIA NIH HHS/ -- R01 AG020961-07/AG/NIA NIH HHS/ -- R01 HL096113/HL/NHLBI NIH HHS/ -- R01 HL096113-03/HL/NHLBI NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA009151-35/CA/NCI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32 HD007249-25/HD/NICHD NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- U01 HL100397-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1078-81. doi: 10.1126/science.1191035. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647425" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Count ; Cell Culture Techniques/*methods ; Cell Death ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Separation ; Cell Survival ; Cells, Cultured ; Elastic Modulus ; Hydrogels ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Muscle Fibers, Skeletal/*cytology/physiology ; Muscle, Skeletal/*cytology ; Polyethylene Glycols ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/cytology/*physiology
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    Loss of Rap1 induces telomere recombination in the absence of NHEJ or a DNA damage signal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Shelterin is an essential telomeric protein complex that prevents DNA damage signaling and DNA repair at mammalian chromosome ends. Here we report on the role of the TRF2-interacting factor Rap1, a conserved shelterin subunit of unknown function. We removed Rap1 from mouse telomeres either through gene deletion or by replacing TRF2 with a mutant that does not bind Rap1. Rap1 was dispensable for the essential functions of TRF2--repression of ATM kinase signaling and nonhomologous end joining (NHEJ)--and mice lacking telomeric Rap1 were viable and fertile. However, Rap1 was critical for the repression of homology-directed repair (HDR), which can alter telomere length. The data reveal that HDR at telomeres can take place in the absence of DNA damage foci and underscore the functional compartmentalization within shelterin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- Kabir, Shaheen -- van Overbeek, Megan -- Celli, Giulia B -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1657-61. doi: 10.1126/science.1185100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339076" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Checkpoint Kinase 2 ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Gene Deletion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Recombination, Genetic ; Signal Transduction ; Sister Chromatid Exchange ; Telomere/*genetics/metabolism ; Telomere-Binding Proteins/chemistry/*genetics/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
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    Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed in models of obesity and type 2 diabetes. Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the c-Jun N-terminal kinase signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132938/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouchi, Noriyuki -- Higuchi, Akiko -- Ohashi, Koji -- Oshima, Yuichi -- Gokce, Noyan -- Shibata, Rei -- Akasaki, Yuichi -- Shimono, Akihiko -- Walsh, Kenneth -- AG15052/AG/NIA NIH HHS/ -- AG34972/AG/NIA NIH HHS/ -- HL81587/HL/NHLBI NIH HHS/ -- HL86785/HL/NHLBI NIH HHS/ -- P01 HL081587/HL/NHLBI NIH HHS/ -- P01 HL081587-05/HL/NHLBI NIH HHS/ -- R01 AG015052/AG/NIA NIH HHS/ -- R01 AG015052-06/AG/NIA NIH HHS/ -- R01 AG034972/AG/NIA NIH HHS/ -- R01 AG034972-03/AG/NIA NIH HHS/ -- R01 HL086785/HL/NHLBI NIH HHS/ -- R01 HL086785-19/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):454-7. doi: 10.1126/science.1188280. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology and Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA. nouchi@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558665" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3-L1 Cells ; Adipocytes/*metabolism/pathology ; Adipokines/genetics/*metabolism ; Adipose Tissue/*metabolism/pathology ; Animals ; Dietary Fats/administration & dosage ; Dietary Sucrose/administration & dosage ; Fatty Liver/pathology/therapy ; Genetic Vectors ; Glucose/metabolism ; Humans ; Inflammation ; Insulin/metabolism ; Insulin Resistance ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Macrophages/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogen-Activated Protein Kinase 8/genetics/metabolism ; Obesity/*metabolism/pathology ; Phosphorylation ; Rats ; Rats, Zucker ; Signal Transduction ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
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    Essential role of the histone methyltransferase G9a in cocaine-induced plasticity (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-09
    Description: Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region, which was regulated by the cocaine-induced transcription factor DeltaFosB. Using conditional mutagenesis and viral-mediated gene transfer, we found that G9a down-regulation increased the dendritic spine plasticity of nucleus accumbens neurons and enhanced the preference for cocaine, thereby establishing a crucial role for histone methylation in the long-term actions of cocaine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maze, Ian -- Covington, Herbert E 3rd -- Dietz, David M -- LaPlant, Quincey -- Renthal, William -- Russo, Scott J -- Mechanic, Max -- Mouzon, Ezekiell -- Neve, Rachael L -- Haggarty, Stephen J -- Ren, Yanhua -- Sampath, Srihari C -- Hurd, Yasmin L -- Greengard, Paul -- Tarakhovsky, Alexander -- Schaefer, Anne -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-120001/DA/NIDA NIH HHS/ -- P01 DA008227-129001/DA/NIDA NIH HHS/ -- P01 DA008227-13/DA/NIDA NIH HHS/ -- P01 DA008227-14/DA/NIDA NIH HHS/ -- P01 DA008227-15/DA/NIDA NIH HHS/ -- P01 DA008227-16/DA/NIDA NIH HHS/ -- P01 DA008227-170003/DA/NIDA NIH HHS/ -- P01 DA008227-180003/DA/NIDA NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P01 DA010044-15/DA/NIDA NIH HHS/ -- P01 DA010044-150005/DA/NIDA NIH HHS/ -- P01 DA010044-159002/DA/NIDA NIH HHS/ -- P01 DA08227/DA/NIDA NIH HHS/ -- P0110044/PHS HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-02/DA/NIDA NIH HHS/ -- R01 DA007359-17/DA/NIDA NIH HHS/ -- R01 DA007359-18/DA/NIDA NIH HHS/ -- R01 DA007359-19/DA/NIDA NIH HHS/ -- R01 DA007359-20/DA/NIDA NIH HHS/ -- R01 DA007359-21/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA07359/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):213-6. doi: 10.1126/science.1179438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
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    Induction of lymphoidlike stroma and immune escape by tumors that express the chemokine CCL21 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Tumor manipulation of host immunity is important for tumor survival and invasion. Many cancers secrete CCL21, a chemoattractant for various leukocytes and lymphoid tissue inducer cells, which drive lymphoid neogenesis. CCL21 expression by melanoma tumors in mice was associated with an immunotolerant microenvironment, which included the induction of lymphoid-like reticular stromal networks, an altered cytokine milieu, and the recruitment of regulatory leukocyte populations. In contrast, CCL21-deficient tumors induced antigen-specific immunity. CCL21-mediated immune tolerance was dependent on host rather than tumor expression of the CCL21 receptor, CCR7, and could protect distant, coimplanted CCL21-deficient tumors and even nonsyngeneic allografts from rejection. We suggest that by altering the tumor microenvironment, CCL21-secreting tumors shift the host immune response from immunogenic to tolerogenic, which facilitates tumor progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shields, Jacqueline D -- Kourtis, Iraklis C -- Tomei, Alice A -- Roberts, Joanna M -- Swartz, Melody A -- New York, N.Y. -- Science. 2010 May 7;328(5979):749-52. doi: 10.1126/science.1185837. Epub 2010 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Chemokine CCL21/*metabolism ; Cytokines/metabolism ; Disease Progression ; Female ; Immune Tolerance ; Lymph Nodes/immunology ; Lymphoid Tissue/*immunology/pathology ; Melanoma, Experimental/*immunology/*pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; RNA Interference ; Receptors, CCR7/metabolism ; Signal Transduction ; Stromal Cells/*immunology/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/immunology ; *Tumor Escape
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Leukotriene A(4) hydrolase (LTA(4)H) is a proinflammatory enzyme that generates the inflammatory mediator leukotriene B(4) (LTB(4)). LTA(4)H also possesses aminopeptidase activity with unknown substrate and physiological importance; we identified the neutrophil chemoattractant proline-glycine-proline (PGP) as this physiological substrate. PGP is a biomarker for chronic obstructive pulmonary disease (COPD) and is implicated in neutrophil persistence in the lung. In acute neutrophil-driven inflammation, PGP was degraded by LTA(4)H, which facilitated the resolution of inflammation. In contrast, cigarette smoke, a major risk factor for the development of COPD, selectively inhibited LTA(4)H aminopeptidase activity, which led to the accumulation of PGP and neutrophils. These studies imply that therapeutic strategies inhibiting LTA(4)H to prevent LTB(4) generation may not reduce neutrophil recruitment because of elevated levels of PGP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snelgrove, Robert J -- Jackson, Patricia L -- Hardison, Matthew T -- Noerager, Brett D -- Kinloch, Andrew -- Gaggar, Amit -- Shastry, Suresh -- Rowe, Steven M -- Shim, Yun M -- Hussell, Tracy -- Blalock, J Edwin -- 082727/Z/07/Z/Wellcome Trust/United Kingdom -- 1K23DK075788/DK/NIDDK NIH HHS/ -- 1R03DK084110-01/DK/NIDDK NIH HHS/ -- G0400795/Medical Research Council/United Kingdom -- G0802752/Medical Research Council/United Kingdom -- HL07783/HL/NHLBI NIH HHS/ -- HL087824/HL/NHLBI NIH HHS/ -- HL090999/HL/NHLBI NIH HHS/ -- HL102371-A1/HL/NHLBI NIH HHS/ -- K08HL091127/HL/NHLBI NIH HHS/ -- P171/03/C1/048/Medical Research Council/United Kingdom -- P30 DK079337/DK/NIDDK NIH HHS/ -- P30AR050948/AR/NIAMS NIH HHS/ -- P30CA13148/CA/NCI NIH HHS/ -- P50 AT00477/AT/NCCIH NIH HHS/ -- R01 HL077783/HL/NHLBI NIH HHS/ -- R01 HL077783-05/HL/NHLBI NIH HHS/ -- R01 HL087824/HL/NHLBI NIH HHS/ -- R01 HL087824-02/HL/NHLBI NIH HHS/ -- R01 HL090999/HL/NHLBI NIH HHS/ -- R01 HL090999-02S1/HL/NHLBI NIH HHS/ -- R01 HL090999-04/HL/NHLBI NIH HHS/ -- R01 HL102371/HL/NHLBI NIH HHS/ -- RR19231/RR/NCRR NIH HHS/ -- U54CA100949/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):90-4. doi: 10.1126/science.1190594. Epub 2010 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham Lung Health Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. rjs198@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813919" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Cells, Cultured ; Chemokines, CXC/metabolism ; Chemotaxis, Leukocyte ; Epoxide Hydrolases/antagonists & inhibitors/isolation & purification/*metabolism ; Female ; Humans ; Inflammation ; Leukotriene B4/metabolism ; Lung/*immunology/metabolism/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/enzymology/immunology/*physiology ; Oligopeptides/*metabolism ; Orthomyxoviridae Infections/immunology/metabolism/pathology ; Pneumococcal Infections/immunology/metabolism/pathology ; Pneumonia/*immunology/metabolism/pathology/therapy ; Proline/*analogs & derivatives/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology/metabolism/pathology ; *Smoke ; Tobacco
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    The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in AML (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Leukemia stem cells (LSCs) are capable of limitless self-renewal and are responsible for the maintenance of leukemia. Because selective eradication of LSCs could offer substantial therapeutic benefit, there is interest in identifying the signaling pathways that control their development. We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpression of the Hoxa9 and Meis1a oncogenes or by the fusion oncoprotein MLL-AF9. We show that the Wnt/beta-catenin signaling pathway is required for self-renewal of LSCs that are derived from either hematopoietic stem cells (HSC) or more differentiated granulocyte-macrophage progenitors (GMP). Because the Wnt/beta-catenin pathway is normally active in HSCs but not in GMP, these results suggest that reactivation of beta-catenin signaling is required for the transformation of progenitor cells by certain oncogenes. beta-catenin is not absolutely required for self-renewal of adult HSCs; thus, targeting the Wnt/beta-catenin pathway may represent a new therapeutic opportunity in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084586/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yingzi -- Krivtsov, Andrei V -- Sinha, Amit U -- North, Trista E -- Goessling, Wolfram -- Feng, Zhaohui -- Zon, Leonard I -- Armstrong, Scott A -- 5P01CA66996/CA/NCI NIH HHS/ -- 5R01HL048801/HL/NHLBI NIH HHS/ -- P01 CA066996/CA/NCI NIH HHS/ -- P01 CA066996-11A1/CA/NCI NIH HHS/ -- R01 HL048801/HL/NHLBI NIH HHS/ -- R01 HL048801-16/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1650-3. doi: 10.1126/science.1186624.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Transformation, Neoplastic ; Genes, Homeobox ; Granulocyte-Macrophage Progenitor Cells/metabolism/pathology ; Hematopoietic Stem Cells/*metabolism/pathology ; Homeodomain Proteins/genetics ; Indomethacin/pharmacology ; Leukemia, Myeloid, Acute/*metabolism/*pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Proteins/genetics ; Neoplastic Stem Cells/*pathology ; *Signal Transduction ; Transduction, Genetic ; Wnt Proteins/*metabolism ; beta Catenin/*metabolism
    Print ISSN: 0036-8075
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    Cortical plasticity induced by inhibitory neuron transplantation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: Critical periods are times of pronounced brain plasticity. During a critical period in the postnatal development of the visual cortex, the occlusion of one eye triggers a rapid reorganization of neuronal responses, a process known as ocular dominance plasticity. We have shown that the transplantation of inhibitory neurons induces ocular dominance plasticity after the critical period. Transplanted inhibitory neurons receive excitatory synapses, make inhibitory synapses onto host cortical neurons, and promote plasticity when they reach a cellular age equivalent to that of endogenous inhibitory neurons during the normal critical period. These findings suggest that ocular dominance plasticity is regulated by the execution of a maturational program intrinsic to inhibitory neurons. By inducing plasticity, inhibitory neuron transplantation may facilitate brain repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164148/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Froemke, Robert C -- Alvarez-Buylla, Arturo -- Stryker, Michael P -- Gandhi, Sunil P -- EY016317/EY/NEI NIH HHS/ -- F32 EY016317/EY/NEI NIH HHS/ -- F32 EY016317-03/EY/NEI NIH HHS/ -- P50 MH077972/MH/NIMH NIH HHS/ -- P50 MH077972-05/MH/NIMH NIH HHS/ -- R01 NS048528/NS/NINDS NIH HHS/ -- R01 NS048528-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1145-8. doi: 10.1126/science.1183962.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; *Dominance, Ocular ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; *Neuronal Plasticity ; Neurons/*transplantation ; Prosencephalon/cytology/embryology ; Sensory Deprivation ; Synapses/physiology ; Visual Cortex/growth & development/*physiology
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    Hippocampal short- and long-term plasticity are not modulated by astrocyte Ca2+ signaling (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-06
    Description: The concept that astrocytes release neuroactive molecules (gliotransmitters) to affect synaptic transmission has been a paradigm shift in neuroscience research over the past decade. This concept suggests that astrocytes, together with pre- and postsynaptic neuronal elements, make up a functional synapse. Astrocyte release of gliotransmitters (for example, glutamate and adenosine triphosphate) is generally accepted to be a Ca2+-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic Gq G protein-coupled receptor Ca2+ signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca2+ fluxes affects spontaneous and evoked excitatory synaptic transmission or synaptic plasticity. Our findings suggest that, at least in the hippocampus, the mechanisms of gliotransmission need to be reconsidered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agulhon, Cendra -- Fiacco, Todd A -- McCarthy, Ken D -- NS020212/NS/NINDS NIH HHS/ -- NS033938/NS/NINDS NIH HHS/ -- R01 NS020212/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1250-4. doi: 10.1126/science.1184821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina at Chapel Hill, Genetic Medicine Building, CB 7365, Chapel Hill, NC 27599, USA. cendra_agulhon@med.unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; CA1 Region, Hippocampal/cytology/*physiology ; Calcium/*metabolism ; *Calcium Signaling ; Excitatory Postsynaptic Potentials ; GTP-Binding Protein alpha Subunits, Gq-G11/metabolism ; In Vitro Techniques ; *Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; N-Methylaspartate/metabolism ; *Neuronal Plasticity ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Synaptic Transmission
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    O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both extracellular matrix proteins containing laminin-G domains and certain arenaviruses. Receptor binding is thought to be mediated by a posttranslational modification, and defective binding with laminin underlies a subclass of congenital muscular dystrophy. Using mass spectrometry- and nuclear magnetic resonance (NMR)-based structural analyses, we identified a phosphorylated O-mannosyl glycan on the mucin-like domain of recombinant alpha-DG, which was required for laminin binding. We demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy, commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein. These findings expand our understanding of the mechanisms that underlie congenital muscular dystrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978000/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshida-Moriguchi, Takako -- Yu, Liping -- Stalnaker, Stephanie H -- Davis, Sarah -- Kunz, Stefan -- Madson, Michael -- Oldstone, Michael B A -- Schachter, Harry -- Wells, Lance -- Campbell, Kevin P -- 1U54NS053672/NS/NINDS NIH HHS/ -- AI55540/AI/NIAID NIH HHS/ -- P30 DK 54759/DK/NIDDK NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P41 RR018502/RR/NCRR NIH HHS/ -- R01 AI009484/AI/NIAID NIH HHS/ -- R01 AI009484-40/AI/NIAID NIH HHS/ -- R01 AI009484-41/AI/NIAID NIH HHS/ -- R01 AI045927/AI/NIAID NIH HHS/ -- R01 AI045927-08/AI/NIAID NIH HHS/ -- R01 AI045927-09/AI/NIAID NIH HHS/ -- R01 AI045927-10/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):88-92. doi: 10.1126/science.1180512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa Roy J. and Lucille A. Carver College of Medicine, 4283 Carver Biomedical Research Building, 285 Newton Road, Iowa City, IA 52242-1101, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044576" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Conformation ; Cell Line ; Dystroglycans/chemistry/*metabolism ; Glycosylation ; Humans ; Laminin/*metabolism ; Magnetic Resonance Spectroscopy ; Mannose/*metabolism ; Mass Spectrometry ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Muscular Dystrophies/metabolism ; Muscular Dystrophy, Animal/metabolism ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Phosphorylation ; Protein Binding ; Recombinant Proteins/chemistry/metabolism
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    Lynx1, a cholinergic brake, limits plasticity in adult visual cortex (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-13
    Description: Experience-dependent brain plasticity typically declines after an early critical period during which circuits are established. Loss of plasticity with closure of the critical period limits improvement of function in adulthood, but the mechanisms that change the brain's plasticity remain poorly understood. Here, we identified an increase in expression of Lynx1 protein in mice that prevented plasticity in the primary visual cortex late in life. Removal of this molecular brake enhanced nicotinic acetylcholine receptor signaling. Lynx1 expression thus maintains stability of mature cortical networks in the presence of cholinergic innervation. The results suggest that modulating the balance between excitatory and inhibitory circuits reactivates visual plasticity and may present a therapeutic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387538/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387538/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morishita, Hirofumi -- Miwa, Julie M -- Heintz, Nathaniel -- Hensch, Takao K -- 1 DP1 OD003699-01/OD/NIH HHS/ -- DA-17279/DA/NIDA NIH HHS/ -- DP1 OD003699/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1238-40. doi: 10.1126/science.1195320. Epub 2010 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉FM Kirby Neurobiology Center, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071629" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amblyopia/metabolism ; Animals ; Cholinesterase Inhibitors/pharmacology ; Dominance, Ocular ; Evoked Potentials, Visual ; Mecamylamine/pharmacology ; Membrane Glycoproteins/*genetics/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neural Inhibition ; *Neuronal Plasticity ; Neuropeptides/*genetics/metabolism/*physiology ; Nicotinic Antagonists/pharmacology ; Physostigmine/pharmacology ; Receptors, Nicotinic/genetics/*metabolism ; Sensory Deprivation ; Signal Transduction ; *Vision, Ocular ; Visual Cortex/*physiology ; Visual Pathways
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    Predicting a human gut microbiota's response to diet in gnotobiotic mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-21
    Description: The interrelationships between our diets and the structure and operations of our gut microbial communities are poorly understood. A model community of 10 sequenced human gut bacteria was introduced into gnotobiotic mice, and changes in species abundance and microbial gene expression were measured in response to randomized perturbations of four defined ingredients in the host diet. From the responses, we developed a statistical model that predicted over 60% of the variation in species abundance evoked by diet perturbations, and we were able to identify which factors in the diet best explained changes seen for each community member. The approach is generally applicable, as shown by a follow-up study involving diets containing various mixtures of pureed human baby foods.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303606/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faith, Jeremiah J -- McNulty, Nathan P -- Rey, Federico E -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-08/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- R37 DK030292-31/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):101-4. doi: 10.1126/science.1206025. Epub 2011 May 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/genetics/physiology ; Biomass ; Caseins/administration & dosage ; Desulfovibrio/genetics/physiology ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats, Unsaturated/administration & dosage ; Dietary Proteins/administration & dosage ; Dietary Sucrose/administration & dosage ; Escherichia coli/genetics/physiology ; Feces/*microbiology ; Gastrointestinal Tract/*microbiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; *Germ-Free Life ; Gram-Negative Bacteria/*physiology ; Gram-Positive Bacteria/genetics/*physiology ; Humans ; Infant ; Infant Food ; Linear Models ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Animal
    Print ISSN: 0036-8075
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    Cerebellum shapes hippocampal spatial code (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-10-25
    Description: Spatial representation is an active process that requires complex multimodal integration from a large interacting network of cortical and subcortical structures. We sought to determine the role of cerebellar protein kinase C (PKC)-dependent plasticity in spatial navigation by recording the activity of hippocampal place cells in transgenic L7PKCI mice with selective disruption of PKC-dependent plasticity at parallel fiber-Purkinje cell synapses. Place cell properties were exclusively impaired when L7PKCI mice had to rely on self-motion cues. The behavioral consequence of such a deficit is evidenced here by selectively impaired navigation capabilities during a path integration task. Together, these results suggest that cerebellar PKC-dependent mechanisms are involved in processing self-motion signals essential to the shaping of hippocampal spatial representation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rochefort, Christelle -- Arabo, Arnaud -- Andre, Marion -- Poucet, Bruno -- Save, Etienne -- Rondi-Reig, Laure -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):385-9. doi: 10.1126/science.1207403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiologie des Processus Adaptatifs (UMR 7102), Navigation, Memory, and Aging (ENMVI) Team, Universite Pierre et Marie Curie-Centre National de la Recherche Scientifique (CNRS), F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/cytology/*physiology ; Cerebellum/enzymology/*physiology ; Cues ; Darkness ; *Long-Term Synaptic Depression ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Motor Activity ; *Orientation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Purkinje Cells/physiology ; Pyramidal Cells/*physiology ; *Space Perception
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A circadian rhythm orchestrated by histone deacetylase 3 controls hepatic lipid metabolism (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-03-12
    Description: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbalpha. Rev-erbalpha colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbalpha in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbalpha directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Dan -- Liu, Tao -- Sun, Zheng -- Bugge, Anne -- Mullican, Shannon E -- Alenghat, Theresa -- Liu, X Shirley -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- HG4069/HG/NHGRI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-20/DK/NIDDK NIH HHS/ -- RC1 DK086239/DK/NIDDK NIH HHS/ -- RC1DK08623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Chromatin Immunoprecipitation ; Chronobiology Disorders/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; DNA/metabolism ; Epigenesis, Genetic ; Fatty Liver/*metabolism ; Gene Expression Regulation ; *Genome ; Histone Deacetylases/*metabolism ; Histones/metabolism ; Homeostasis ; *Lipid Metabolism ; Lipogenesis/genetics ; Liver/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Receptor Co-Repressor 1/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/metabolism ; RNA Polymerase II/metabolism ; Up-Regulation
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    Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253482/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ives, Annette -- Ronet, Catherine -- Prevel, Florence -- Ruzzante, Giulia -- Fuertes-Marraco, Silvia -- Schutz, Frederic -- Zangger, Haroun -- Revaz-Breton, Melanie -- Lye, Lon-Fye -- Hickerson, Suzanne M -- Beverley, Stephen M -- Acha-Orbea, Hans -- Launois, Pascal -- Fasel, Nicolas -- Masina, Slavica -- A129646/PHS HHS/ -- R01 AI029646/AI/NIAID NIH HHS/ -- R01 AI029646-23/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):775-8. doi: 10.1126/science.1199326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokines/*metabolism ; Cytokines/*metabolism ; Inflammation Mediators/metabolism ; Leishmania guyanensis/*pathogenicity/*virology ; Leishmaniasis, Mucocutaneous/*immunology/parasitology ; Leishmaniavirus/*immunology/physiology ; Macrophages/immunology/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Parasitemia ; Phagosomes/parasitology ; RNA, Double-Stranded/immunology ; RNA, Viral/immunology ; Toll-Like Receptor 3/*immunology ; Toll-Like Receptors/immunology
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    A gustotopic map of taste qualities in the mammalian brain (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. We explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty qualities are represented in the primary taste cortex of mice. We used in vivo two-photon calcium imaging to demonstrate topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523322/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523322/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xiaoke -- Gabitto, Mariano -- Peng, Yueqing -- Ryba, Nicholas J P -- Zuker, Charles S -- Z01 DE000561-15/Intramural NIH HHS/ -- Z01 DE000561-16/Intramural NIH HHS/ -- ZIA DE000561-17/Intramural NIH HHS/ -- ZIA DE000561-18/Intramural NIH HHS/ -- ZIA DE000561-19/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1262-6. doi: 10.1126/science.1204076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885776" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; *Brain Mapping ; Cerebral Cortex/cytology/*physiology ; Cycloheximide ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Imaging ; Neurons/*physiology ; Sodium Chloride ; Sodium Glutamate ; Sweetening Agents ; Taste/*physiology ; Taste Buds/physiology
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    The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-23
    Description: Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Round, June L -- Lee, S Melanie -- Li, Jennifer -- Tran, Gloria -- Jabri, Bana -- Chatila, Talal A -- Mazmanian, Sarkis K -- AI 080002/AI/NIAID NIH HHS/ -- AI 088626/AI/NIAID NIH HHS/ -- DK 078938/DK/NIDDK NIH HHS/ -- DK 083633/DK/NIDDK NIH HHS/ -- R01 AI085090/AI/NIAID NIH HHS/ -- R01 AI085090-01/AI/NIAID NIH HHS/ -- R01 AI085090-01S1/AI/NIAID NIH HHS/ -- R01 AI085090-02/AI/NIAID NIH HHS/ -- R01 AI085090-03/AI/NIAID NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI080002/AI/NIAID NIH HHS/ -- R21 AI080002-01/AI/NIAID NIH HHS/ -- R21 AI080002-02/AI/NIAID NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):974-7. doi: 10.1126/science.1206095. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. jround@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides fragilis/*growth & development/*immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; Humans ; *Immune Tolerance ; Immunity, Mucosal ; Interleukin-10/metabolism ; Intestinal Mucosa/*immunology/*microbiology ; Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Polysaccharides, Bacterial/immunology/*metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms ; Symbiosis ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Toll-Like Receptor 2/immunology/*metabolism
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    Endocannabinoid hydrolysis generates brain prostaglandins that promote neuroinflammation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Phospholipase A(2)(PLA(2)) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol to generate a major arachidonate precursor pool for neuroinflammatory prostaglandins. MAGL-disrupted animals show neuroprotection in a parkinsonian mouse model. These animals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are instead regulated by cytosolic PLA(2). These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nomura, Daniel K -- Morrison, Bradley E -- Blankman, Jacqueline L -- Long, Jonathan Z -- Kinsey, Steven G -- Marcondes, Maria Cecilia G -- Ward, Anna M -- Hahn, Yun Kyung -- Lichtman, Aron H -- Conti, Bruno -- Cravatt, Benjamin F -- 5P01DA009789/DA/NIDA NIH HHS/ -- AG028040/AG/NIA NIH HHS/ -- DA017259/DA/NIDA NIH HHS/ -- DA026261/DA/NIDA NIH HHS/ -- F31 DA026261-03/DA/NIDA NIH HHS/ -- K99 DA030908/DA/NIDA NIH HHS/ -- K99 DA030908-01/DA/NIDA NIH HHS/ -- K99DA030908/DA/NIDA NIH HHS/ -- P01 DA009789/DA/NIDA NIH HHS/ -- P01 DA009789-14/DA/NIDA NIH HHS/ -- P01 DA017259/DA/NIDA NIH HHS/ -- P01 DA017259-08/DA/NIDA NIH HHS/ -- P01DA01725/DA/NIDA NIH HHS/ -- R00 DA030908/DA/NIDA NIH HHS/ -- R00 DA030908-02/DA/NIDA NIH HHS/ -- R00DA030908/DA/NIDA NIH HHS/ -- R01 AG028040/AG/NIA NIH HHS/ -- R01 AG028040-04/AG/NIA NIH HHS/ -- R03 DA027936/DA/NIDA NIH HHS/ -- R03 DA027936-02/DA/NIDA NIH HHS/ -- R03DA027936/DA/NIDA NIH HHS/ -- T32 DA007027/DA/NIDA NIH HHS/ -- T32 DA007027-33/DA/NIDA NIH HHS/ -- T32DA007027/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):809-13. doi: 10.1126/science.1209200. Epub 2011 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. dnomura@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021672" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acid/metabolism ; Arachidonic Acids/*metabolism ; Benzodioxoles/pharmacology ; Brain/drug effects/*metabolism/pathology ; Cannabinoid Receptor Modulators/*metabolism ; Cyclooxygenase 1/metabolism ; Cytokines/metabolism ; Eicosanoids/metabolism ; *Endocannabinoids ; Enzyme Inhibitors/pharmacology ; Glycerides/*metabolism ; Hydrolysis ; Inflammation/*metabolism/pathology ; Inflammation Mediators/pharmacology ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Lung/metabolism ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/antagonists & inhibitors/genetics/*metabolism ; Neuroprotective Agents/pharmacology ; Parkinsonian Disorders/metabolism/pathology ; Phospholipases A2/genetics/metabolism ; Piperidines/pharmacology ; Prostaglandins/biosynthesis/*metabolism ; Signal Transduction
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    Different B cell populations mediate early and late memory during an endogenous immune response (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: Memory B cells formed in response to microbial antigens provide immunity to later infections; however, the inability to detect rare endogenous antigen-specific cells limits current understanding of this process. Using an antigen-based technique to enrich these cells, we found that immunization with a model protein generated B memory cells that expressed isotype-switched immunoglobulins (swIg) or retained IgM. The more numerous IgM(+) cells were longer lived than the swIg(+) cells. However, swIg(+) memory cells dominated the secondary response because of the capacity to become activated in the presence of neutralizing serum immunoglobulin. Thus, we propose that memory relies on swIg(+) cells until they disappear and serum immunoglobulin falls to a low level, in which case memory resides with durable IgM(+) reserves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pape, Kathryn A -- Taylor, Justin J -- Maul, Robert W -- Gearhart, Patricia J -- Jenkins, Marc K -- F32 AI091033/AI/NIAID NIH HHS/ -- R01 AI036914/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R37 AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1203-7. doi: 10.1126/science.1201730. Epub 2011 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD38/analysis ; B-Lymphocyte Subsets/*immunology ; Cell Survival ; Female ; Germinal Center/cytology/immunology ; Immunization ; *Immunoglobulin Class Switching ; Immunoglobulin M/genetics/*immunology ; *Immunologic Memory ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phycocyanin/immunology ; Phycoerythrin/immunology ; Spleen/cytology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-01
    Description: Lymphocytes egress from lymphoid organs in response to sphingosine-1-phosphate (S1P); minutes later they migrate from blood into tissue against the S1P gradient. The mechanisms facilitating cell movement against the gradient have not been defined. Here, we show that heterotrimeric guanine nucleotide-binding protein-coupled receptor kinase-2 (GRK2) functions in down-regulation of S1P receptor-1 (S1PR1) on blood-exposed lymphocytes. T and B cell movement from blood into lymph nodes is reduced in the absence of GRK2 but is restored in S1P-deficient mice. In the spleen, B cell movement between the blood-rich marginal zone and follicles is disrupted by GRK2 deficiency and by mutation of an S1PR1 desensitization motif. Moreover, delivery of systemic antigen into follicles is impaired. Thus, GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate into lymphoid tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267326/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267326/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnon, Tal I -- Xu, Ying -- Lo, Charles -- Pham, Trung -- An, Jinping -- Coughlin, Shaun -- Dorn, Gerald W -- Cyster, Jason G -- AI74847/AI/NIAID NIH HHS/ -- R01 AI074847/AI/NIAID NIH HHS/ -- R01 AI074847-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 30;333(6051):1898-903. doi: 10.1126/science.1208248.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21960637" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/immunology ; B-Lymphocytes/immunology/*physiology ; Blood ; Cell Movement ; Chemokines/physiology ; Chemotaxis, Leukocyte ; Down-Regulation ; G-Protein-Coupled Receptor Kinase 2/*metabolism ; Ligands ; Lymph Nodes/cytology ; Lysophospholipids/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Receptors, Lysosphingolipid/genetics/*metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives/metabolism ; Spleen/cytology/immunology ; T-Lymphocytes/immunology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of visual pigments by light and heat (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-11
    Description: Vision begins with photoisomerization of visual pigments. Thermal energy can complement photon energy to drive photoisomerization, but it also triggers spontaneous pigment activation as noise that interferes with light detection. For half a century, the mechanism underlying this dark noise has remained controversial. We report here a quantitative relation between a pigment's photoactivation energy and its peak-absorption wavelength, lambda(max). Using this relation and assuming that pigment activations by light and heat go through the same ground-state isomerization energy barrier, we can predict the relative noise of diverse pigments with multi-vibrational-mode thermal statistics. The agreement between predictions and our measurements strongly suggests that pigment noise arises from canonical isomerization. The predicted high noise for pigments with lambda(max) in the infrared presumably explains why they apparently do not exist in nature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349410/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luo, Dong-Gen -- Yue, Wendy W S -- Ala-Laurila, Petri -- Yau, King-Wai -- EY06837/EY/NEI NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jun 10;332(6035):1307-12. doi: 10.1126/science.1200172.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dgluo@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21659602" target="_blank"〉PubMed〈/a〉
    Keywords: Ambystoma ; Animals ; Bufo marinus ; Goldfish ; Hot Temperature ; In Vitro Techniques ; Light ; *Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Photons ; Retinal Cone Photoreceptor Cells/physiology ; Retinal Pigments/chemistry/*physiology/radiation effects ; Rhodopsin/physiology
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    The antibacterial lectin RegIIIgamma promotes the spatial segregation of microbiota and host in the intestine (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. The proximity of vast numbers of bacteria to host intestinal tissues raises the question of how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show that RegIIIgamma, a secreted antibacterial lectin, is essential for maintaining a ~50-micrometer zone that physically separates the microbiota from the small intestinal epithelial surface. Loss of host-bacterial segregation in RegIIIgamma(-/-) mice was coupled to increased bacterial colonization of the intestinal epithelial surface and enhanced activation of intestinal adaptive immune responses by the microbiota. Together, our findings reveal that RegIIIgamma is a fundamental immune mechanism that promotes host-bacterial mutualism by regulating the spatial relationships between microbiota and host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321924/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaishnava, Shipra -- Yamamoto, Miwako -- Severson, Kari M -- Ruhn, Kelly A -- Yu, Xiaofei -- Koren, Omry -- Ley, Ruth -- Wakeland, Edward K -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-06/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):255-8. doi: 10.1126/science.1209791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998396" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Anti-Bacterial Agents/pharmacology ; Bacterial Load ; Gram-Negative Bacteria/immunology/*physiology ; Gram-Positive Bacteria/immunology/*physiology ; Homeostasis ; Immunoglobulin A/analysis ; Intestinal Mucosa/immunology/*microbiology ; Intestine, Small/immunology/*microbiology ; Lectins, C-Type/physiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics/metabolism ; Proteins/*metabolism ; Symbiosis ; T-Lymphocytes, Helper-Inducer/immunology
    Print ISSN: 0036-8075
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    Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-02
    Description: Waves of cyclin synthesis and degradation regulate the activity of Cdc2 protein kinase during the cell cycle. Cdc2 inactivation by Wee1B-mediated phosphorylation is necessary for arrest of the oocyte at G2-prophase, but it is unclear whether this regulation functions later during the metaphase-to-anaphase transition. We show that reactivation of a Wee1B pathway triggers the decrease in Cdc2 activity during egg activation. When Wee1B is down-regulated, oocytes fail to form a pronucleus in response to Ca(2+) signals. Calcium-calmodulin-dependent kinase II (CaMKII) activates Wee1B, and CaMKII-driven exit from metaphase II is inhibited by Wee1B down-regulation, demonstrating that exit from metaphase requires not only a proteolytic degradation of cyclin B but also the inhibitory phosphorylation of Cdc2 by Wee1B.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104668/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, Jeong Su -- Susor, Andrej -- Conti, Marco -- GM080527-05/GM/NIGMS NIH HHS/ -- HD052909/HD/NICHD NIH HHS/ -- R01 GM080527/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):462-5. doi: 10.1126/science.1199211. Epub 2011 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA 94143-0556, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; Calcium/metabolism ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cyclin B/genetics/metabolism ; Down-Regulation ; Female ; Gene Knockdown Techniques ; Maturation-Promoting Factor/metabolism ; *Meiosis ; *Metaphase ; Mice ; Mice, Inbred C57BL ; Oocytes/*physiology ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; RNA, Messenger/genetics/metabolism
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    Successful transmission of a retrovirus depends on the commensal microbiota (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-10-15
    Description: To establish chronic infections, viruses must develop strategies to evade the host's immune responses. Many retroviruses, including mouse mammary tumor virus (MMTV), are transmitted most efficiently through mucosal surfaces rich in microbiota. We found that MMTV, when ingested by newborn mice, stimulates a state of unresponsiveness toward viral antigens. This process required the intestinal microbiota, as antibiotic-treated mice or germ-free mice did not transmit infectious virus to their offspring. MMTV-bound bacterial lipopolysaccharide triggered Toll-like receptor 4 and subsequent interleukin-6 (IL-6)-dependent induction of the inhibitory cytokine IL-10. Thus, MMTV has evolved to rely on the interaction with the microbiota to induce an immune evasion pathway. Together, these findings reveal the fundamental importance of commensal microbiota in viral infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519937/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kane, Melissa -- Case, Laure K -- Kopaskie, Karyl -- Kozlova, Alena -- MacDearmid, Cameron -- Chervonsky, Alexander V -- Golovkina, Tatyana V -- AI082418/AI/NIAID NIH HHS/ -- AI090084/AI/NIAID NIH HHS/ -- CA100383/CA/NCI NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- P30 CA014599/CA/NCI NIH HHS/ -- R01 AI090084/AI/NIAID NIH HHS/ -- R01 CA134667/CA/NCI NIH HHS/ -- R56 AI090084/AI/NIAID NIH HHS/ -- T32 AI065382-01/AI/NIAID NIH HHS/ -- T32GM007183/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):245-9. doi: 10.1126/science.1210718.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anti-Bacterial Agents/pharmacology ; Antibodies, Viral/biosynthesis ; Antigens, Viral/immunology ; *Bacterial Physiological Phenomena ; Female ; Germ-Free Life ; *Immune Evasion ; Interleukin-10/genetics/metabolism ; Intestinal Mucosa/*virology ; Intestines/*microbiology ; Lipopolysaccharides/immunology/metabolism ; Mammary Tumor Virus, Mouse/*immunology/*pathogenicity ; *Metagenome ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Pregnancy ; Pregnancy Complications, Infectious/virology ; Retroviridae Infections/immunology/*transmission/virology ; Specific Pathogen-Free Organisms ; Toll-Like Receptor 4/immunology/metabolism ; Tumor Virus Infections/immunology/transmission/virology ; Virus Replication
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    Role for the membrane receptor guanylyl cyclase-C in attention deficiency and hyperactive behavior (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-13
    Description: Midbrain dopamine neurons regulate many important behavioral processes, and their dysfunctions are associated with several human neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD) and schizophrenia. Here, we report that these neurons in mice selectively express guanylyl cyclase-C (GC-C), a membrane receptor previously thought to be expressed mainly in the intestine. GC-C activation potentiates the excitatory responses mediated by glutamate and acetylcholine receptors via the activity of guanosine 3',5'-monophosphate-dependent protein kinase (PKG). Mice in which GC-C has been knocked out exhibit hyperactivity and attention deficits. Moreover, their behavioral phenotypes are reversed by ADHD therapeutics and a PKG activator. These results indicate important behavioral and physiological functions for the GC-C/PKG signaling pathway within the brain and suggest new therapeutic targets for neuropsychiatric disorders related to the malfunctions of midbrain dopamine neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Rong -- Ding, Cheng -- Hu, Ji -- Lu, Yao -- Liu, Fei -- Mann, Elizabeth -- Xu, Fuqiang -- Cohen, Mitchell B -- Luo, Minmin -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1642-6. doi: 10.1126/science.1207675. Epub 2011 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21835979" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/administration & dosage ; Animals ; Attention ; Attention Deficit Disorder with Hyperactivity/genetics/*metabolism ; Behavior, Animal/drug effects ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/*metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Enzyme Activation ; Gastrointestinal Hormones/metabolism/pharmacology ; Glycine/analogs & derivatives/metabolism/pharmacology ; Impulsive Behavior ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Natriuretic Peptides/metabolism/pharmacology ; Neurons/*metabolism ; Patch-Clamp Techniques ; Receptors, Glutamate/metabolism ; Receptors, Guanylate Cyclase-Coupled/genetics/*metabolism ; Receptors, Muscarinic/metabolism ; Receptors, Peptide/genetics/*metabolism ; Resorcinols/metabolism/pharmacology ; Signal Transduction ; Substantia Nigra/cytology/*metabolism ; Ventral Tegmental Area/cytology/*metabolism
    Print ISSN: 0036-8075
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    Chemical and genetic engineering of selective ion channel-ligand interactions (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: Ionic flux mediates essential physiological and behavioral functions in defined cell populations. Cell type-specific activators of diverse ionic conductances are needed for probing these effects. We combined chemistry and protein engineering to enable the systematic creation of a toolbox of ligand-gated ion channels (LGICs) with orthogonal pharmacologic selectivity and divergent functional properties. The LGICs and their small-molecule effectors were able to activate a range of ionic conductances in genetically specified cell types. LGICs constructed for neuronal perturbation could be used to selectively manipulate neuron activity in mammalian brains in vivo. The diversity of ion channel tools accessible from this approach will be useful for examining the relationship between neuronal activity and animal behavior, as well as for cell biological and physiological applications requiring chemical control of ion conductance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210548/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnus, Christopher J -- Lee, Peter H -- Atasoy, Deniz -- Su, Helen H -- Looger, Loren L -- Sternson, Scott M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1292-6. doi: 10.1126/science.1206606.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/chemistry/metabolism/pharmacology ; Bicyclo Compounds/chemistry/metabolism/pharmacology ; Brain/cytology/physiology ; Feeding Behavior ; Female ; HEK293 Cells ; Humans ; Ion Channel Gating ; Ligand-Gated Ion Channels/chemistry/*genetics/*metabolism ; Ligands ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; Neurons/*physiology ; Patch-Clamp Techniques ; Protein Binding ; *Protein Engineering ; Protein Structure, Tertiary ; Quinuclidines/chemistry/metabolism/pharmacology ; Receptors, Glycine/genetics/metabolism ; Receptors, Nicotinic/chemistry/genetics/metabolism ; Receptors, Serotonin, 5-HT3/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Molecule Libraries ; Stereoisomerism ; alpha7 Nicotinic Acetylcholine Receptor
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    Distinct properties of the XY pseudoautosomal region crucial for male meiosis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: Meiosis requires that each chromosome find its homologous partner and undergo at least one crossover. X-Y chromosome segregation hinges on efficient crossing-over in a very small region of homology, the pseudoautosomal region (PAR). We find that mouse PAR DNA occupies unusually long chromosome axes, potentially as shorter chromatin loops, predicted to promote double-strand break (DSB) formation. Most PARs show delayed appearance of RAD51/DMC1 foci, which mark DSB ends, and all PARs undergo delayed DSB-mediated homologous pairing. Analysis of Spo11beta isoform-specific transgenic mice revealed that late RAD51/DMC1 foci in the PAR are genetically distinct from both early PAR foci and global foci and that late PAR foci promote efficient X-Y pairing, recombination, and male fertility. Our findings uncover specific mechanisms that surmount the unique challenges of X-Y recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151169/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151169/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kauppi, Liisa -- Barchi, Marco -- Baudat, Frederic -- Romanienko, Peter J -- Keeney, Scott -- Jasin, Maria -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-01/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):916-20. doi: 10.1126/science.1195774.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330546" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/metabolism ; Chromatin/chemistry/metabolism ; *Chromosome Pairing ; Chromosome Segregation ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; Endodeoxyribonucleases/genetics/*metabolism ; Female ; In Situ Hybridization, Fluorescence ; Male ; *Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Protein Isoforms ; Rad51 Recombinase/metabolism ; X Chromosome/*physiology ; Y Chromosome/*physiology
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    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lan -- Gural, Alexander -- Sun, Xiao-Jian -- Zhao, Xinyang -- Perna, Fabiana -- Huang, Gang -- Hatlen, Megan A -- Vu, Ly -- Liu, Fan -- Xu, Haiming -- Asai, Takashi -- Xu, Hao -- Deblasio, Tony -- Menendez, Silvia -- Voza, Francesca -- Jiang, Yanwen -- Cole, Philip A -- Zhang, Jinsong -- Melnick, Ari -- Roeder, Robert G -- Nimer, Stephen D -- GM62437/GM/NIGMS NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):765-9. doi: 10.1126/science.1201662. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764752" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; E1A-Associated p300 Protein/antagonists & inhibitors/*metabolism ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoietic Stem Cells/*cytology/physiology ; Humans ; Leukemia, Myeloid, Acute/*metabolism/pathology ; Lysine/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Preleukemia/metabolism/pathology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Transcriptional Activation ; Tumor Cells, Cultured
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    Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368507/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Tomizawa, Shin-ichi -- Mitsuya, Kohzoh -- Totoki, Yasushi -- Yamamoto, Yasuhiro -- Kuramochi-Miyagawa, Satomi -- Iida, Naoko -- Hoki, Yuko -- Murphy, Patrick J -- Toyoda, Atsushi -- Gotoh, Kengo -- Hiura, Hitoshi -- Arima, Takahiro -- Fujiyama, Asao -- Sado, Takashi -- Shibata, Tatsuhiro -- Nakano, Toru -- Lin, Haifan -- Ichiyanagi, Kenji -- Soloway, Paul D -- Sasaki, Hiroyuki -- R01 CA098597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 May 13;332(6031):848-52. doi: 10.1126/science.1203919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics and Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima, Shizuoka, 411-8540, Japan. toshwatatoshiakiwatanabe@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *DNA Methylation ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Proteins/genetics/metabolism ; Models, Genetic ; Mutation ; Phospholipase D/genetics/metabolism ; Proteins/genetics/metabolism ; RNA, Small Interfering/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Spermatogonia/metabolism ; Testis/embryology/metabolism ; Transcription, Genetic ; ras-GRF1/*genetics
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    Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144160/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Davina -- Molofsky, Ari B -- Liang, Hong-Erh -- Ricardo-Gonzalez, Roberto R -- Jouihan, Hani A -- Bando, Jennifer K -- Chawla, Ajay -- Locksley, Richard M -- 5F30DK083194-02/DK/NIDDK NIH HHS/ -- AI026918/AI/NIAID NIH HHS/ -- DK063720/DK/NIDDK NIH HHS/ -- DP1 OD006415/OD/NIH HHS/ -- F30 DK083194-03/DK/NIDDK NIH HHS/ -- R01 AI030663/AI/NIAID NIH HHS/ -- R01 DK076760/DK/NIDDK NIH HHS/ -- R01 DK081405/DK/NIDDK NIH HHS/ -- R01 HL076746/HL/NHLBI NIH HHS/ -- R37 AI026918/AI/NIAID NIH HHS/ -- R37 AI026918-24/AI/NIAID NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):243-7. doi: 10.1126/science.1201475. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436399" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adipose Tissue, White/cytology/*immunology/*metabolism ; Animals ; Blood Glucose/*metabolism ; Cell Movement ; Dietary Fats/administration & dosage ; Eosinophilia/immunology ; Eosinophils/immunology/*physiology ; Glucose Intolerance ; Homeostasis ; Insulin/metabolism ; Insulin Resistance ; Interleukin-13/genetics/metabolism ; Interleukin-4/genetics/metabolism ; *Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Nippostrongylus ; Strongylida Infections/immunology/metabolism
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    Trim28 is required for epigenetic stability during mouse oocyte to embryo transition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1beta), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messerschmidt, Daniel M -- de Vries, Wilhelmine -- Ito, Mitsuteru -- Solter, Davor -- Ferguson-Smith, Anne -- Knowles, Barbara B -- 079249/Wellcome Trust/United Kingdom -- 095606/Wellcome Trust/United Kingdom -- MR/J001597/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1499-502. doi: 10.1126/science.1216154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; DNA Methylation ; Down-Regulation ; *Embryo Loss ; Embryo, Mammalian/*physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Oocytes/*physiology ; Phenotype ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/*genetics/*physiology
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/genetics/metabolism
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    A single progenitor population switches behavior to maintain and repair esophageal epithelium (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-07-24
    Description: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doupe, David P -- Alcolea, Maria P -- Roshan, Amit -- Zhang, Gen -- Klein, Allon M -- Simons, Benjamin D -- Jones, Philip H -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0601740/Medical Research Council/United Kingdom -- G0700600/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U105370181/Medical Research Council/United Kingdom -- U.1053.00.010(70181)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1091-3. doi: 10.1126/science.1218835. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Doxycycline/pharmacology ; Epithelial Cells/*physiology ; Epithelium/drug effects/metabolism/*physiology ; Esophagus/*cytology/*physiology ; Green Fluorescent Proteins/biosynthesis ; Histones/biosynthesis ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/biosynthesis ; *Regeneration ; Stem Cells/metabolism/*physiology
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    Locally synchronized synaptic inputs (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-24
    Description: Synaptic inputs on dendrites are nonlinearly converted to action potential outputs, yet the spatiotemporal patterns of dendritic activation remain to be elucidated at single-synapse resolution. In rodents, we optically imaged synaptic activities from hundreds of dendritic spines in hippocampal and neocortical pyramidal neurons ex vivo and in vivo. Adjacent spines were frequently synchronized in spontaneously active networks, thereby forming dendritic foci that received locally convergent inputs from presynaptic cell assemblies. This precise subcellular geometry manifested itself during N-methyl-D-aspartate receptor-dependent circuit remodeling. Thus, clustered synaptic plasticity is innately programmed to compartmentalize correlated inputs along dendrites and may reify nonlinear synaptic integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, Naoya -- Kitamura, Kazuo -- Matsuo, Naoki -- Mayford, Mark -- Kano, Masanobu -- Matsuki, Norio -- Ikegaya, Yuji -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):353-6. doi: 10.1126/science.1210362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267814" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; CA3 Region, Hippocampal/cytology/physiology ; Calcium/metabolism ; Dendritic Spines/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Net/*physiology ; Neuronal Plasticity ; Organ Culture Techniques ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Somatosensory Cortex/cytology/physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interleukin-22 drives endogenous thymic regeneration in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: Endogenous thymic regeneration is a crucial function that allows for renewal of immune competence after stress, infection, or immunodepletion. However, the mechanisms governing this regeneration remain poorly understood. We detail such a mechanism, centered on interleukin-22 (IL-22) and triggered by the depletion of CD4(+)CD8(+) double-positive thymocytes. Intrathymic levels of IL-22 were increased after thymic insult, and thymic recovery was impaired in IL-22-deficient mice. IL-22, which signaled through thymic epithelial cells and promoted their proliferation and survival, was up-regulated by radio-resistant RORgamma(t)(+)CCR6(+)NKp46(-) lymphoid tissue inducer cells after thymic injury in an IL-23-dependent manner. Administration of IL-22 enhanced thymic recovery after total body irradiation. These studies reveal mechanisms of endogenous thymic repair and offer innovative regenerative strategies for improving immune competence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616391/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudakov, Jarrod A -- Hanash, Alan M -- Jenq, Robert R -- Young, Lauren F -- Ghosh, Arnab -- Singer, Natalie V -- West, Mallory L -- Smith, Odette M -- Holland, Amanda M -- Tsai, Jennifer J -- Boyd, Richard L -- van den Brink, Marcel R M -- AI080455/AI/NIAID NIH HHS/ -- CA107096/CA/NCI NIH HHS/ -- HL069929/HL/NHLBI NIH HHS/ -- HL095075/HL/NHLBI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 CA107096/CA/NCI NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL095075/HL/NHLBI NIH HHS/ -- T32 CA009207/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):91-5. doi: 10.1126/science.1218004. Epub 2012 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. dudakovj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Proliferation ; Cell Survival ; Dendritic Cells/physiology ; Epithelial Cells/cytology/physiology ; Interleukin-23/metabolism ; Interleukins/administration & dosage/deficiency/genetics/*metabolism ; Lymphocytes/cytology/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics/metabolism ; Radiation Dosage ; Receptors, Interleukin/metabolism ; Recombinant Proteins/administration & dosage ; *Regeneration ; Signal Transduction ; Thymocytes/*physiology ; Thymus Gland/cytology/immunology/*physiology/radiation effects ; Up-Regulation ; Whole-Body Irradiation
    Print ISSN: 0036-8075
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    Asymmetric segregation of polarized antigen on B cell division shapes presentation capacity (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-28
    Description: During the activation of humoral immune responses, B cells acquire antigen for subsequent presentation to cognate T cells. Here we show that after mouse B cells accumulate antigen, it is maintained in a polarized distribution for extended periods in vivo. Using high-throughput imaging flow cytometry, we observed that this polarization is preserved during B cell division, promoting asymmetric antigen segregation among progeny. Antigen inheritance correlates with the ability of progeny to activate T cells: Daughter cells receiving larger antigen stores exhibit a prolonged capacity to present antigen, which renders them more effective in competing for T cell help. The generation of progeny with differential capacities for antigen presentation may have implications for somatic hypermutation and class switching during affinity maturation and as B cells commit to effector cell fates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thaunat, Olivier -- Granja, Aitor G -- Barral, Patricia -- Filby, Andrew -- Montaner, Beatriz -- Collinson, Lucy -- Martinez-Martin, Nuria -- Harwood, Naomi E -- Bruckbauer, Andreas -- Batista, Facundo D -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 27;335(6067):475-9. doi: 10.1126/science.1214100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens/*analysis/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Computer Simulation ; Flow Cytometry ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Muramidase/analysis/immunology ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Pheromonal induction of spatial learning in mice (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-12-15
    Description: Many mammals use scent marking for sexual and competitive advertisement, but little is known about the mechanism by which scents are used to locate mates and competitors. We show that darcin, an involatile protein sex pheromone in male mouse urine, can rapidly condition preference for its remembered location among females and competitor males so that animals prefer to spend time in the site even when scent is absent. Learned spatial preference is conditioned through contact with darcin in a single trial and remembered for approximately 14 days. This pheromone-induced learning allows animals to relocate sites of particular social relevance and provides proof that pheromones such as darcin can be highly potent stimuli for social learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Sarah A -- Davidson, Amanda J -- McLean, Lynn -- Beynon, Robert J -- Hurst, Jane L -- BB/J002631/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC503897/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1462-5. doi: 10.1126/science.1225638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Behaviour and Evolution Group, Institute of Integrative Biology, University of Liverpool, Leahurst Campus, Neston CH64 7TE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Competitive Behavior/drug effects/*physiology ; Conditioning (Psychology)/drug effects/physiology ; Female ; Male ; Maze Learning/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Proteins/pharmacology/*physiology ; Sex Attractants/pharmacology/*physiology/urine ; Smell/drug effects/physiology ; Spatial Behavior/drug effects/*physiology
    Print ISSN: 0036-8075
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    Gap junctions compensate for sublinear dendritic integration in an inhibitory network (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-10
    Description: Electrically coupled inhibitory interneurons dynamically control network excitability, yet little is known about how chemical and electrical synapses regulate their activity. Using two-photon glutamate uncaging and dendritic patch-clamp recordings, we found that the dendrites of cerebellar Golgi interneurons acted as passive cables. They conferred distance-dependent sublinear synaptic integration and weakened distal excitatory inputs. Gap junctions were present at a higher density on distal dendrites and contributed substantially to membrane conductance. Depolarization of one Golgi cell increased firing in its neighbors, and inclusion of dendritic gap junctions in interneuron network models enabled distal excitatory synapses to drive network activity more effectively. Our results suggest that dendritic gap junctions counteract sublinear dendritic integration by enabling excitatory synaptic charge to spread into the dendrites of neighboring inhibitory interneurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587282/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vervaeke, Koen -- Lorincz, Andrea -- Nusser, Zoltan -- Silver, R Angus -- 064413/Wellcome Trust/United Kingdom -- 090197/Wellcome Trust/United Kingdom -- 095667/Wellcome Trust/United Kingdom -- 293681/European Research Council/International -- 294667/European Research Council/International -- BB/F005490/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- F005490/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400598/Medical Research Council/United Kingdom -- G0400598(71261)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1624-8. doi: 10.1126/science.1215101. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology and Pharmacology, University College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403180" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Cerebellar Cortex/cytology ; Computer Simulation ; Dendrites/*physiology/*ultrastructure ; Electrical Synapses/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Interneurons/*physiology ; Ion Channels/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Neurological ; Nerve Net/*physiology/ultrastructure ; *Neural Inhibition ; Patch-Clamp Techniques ; Synapses/physiology ; Synaptic Transmission
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    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/physiology
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    Regulated virulence controls the ability of a pathogen to compete with the gut microbiota (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-15
    Description: The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439148/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamada, Nobuhiko -- Kim, Yun-Gi -- Sham, Ho Pan -- Vallance, Bruce A -- Puente, Jose L -- Martens, Eric C -- Nunez, Gabriel -- DK091191/DK/NIDDK NIH HHS/ -- DK61707/DK/NIDDK NIH HHS/ -- R01 DK061707/DK/NIDDK NIH HHS/ -- R01 DK091191/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1325-9. doi: 10.1126/science.1222195. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Load ; Bacterial Proteins/genetics/metabolism ; Bacteroides/*growth & development ; Citrobacter rodentium/genetics/growth & development/immunology/*pathogenicity ; Enterobacteriaceae Infections/immunology/*microbiology ; Escherichia coli/*growth & development ; Feces/microbiology ; Gene Expression Regulation, Bacterial ; Germ-Free Life ; Intestinal Mucosa/*microbiology ; Intestines/*microbiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; *Microbial Interactions ; Specific Pathogen-Free Organisms ; Virulence Factors/genetics/metabolism
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    Glucocorticoids can induce PTSD-like memory impairments in mice (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-01
    Description: Posttraumatic stress disorder (PTSD) is characterized by a hypermnesia of the trauma and by a memory impairment that decreases the ability to restrict fear to the appropriate context. Infusion of glucocorticoids in the hippocampus after fear conditioning induces PTSD-like memory impairments and an altered pattern of neural activation in the hippocampal-amygdalar circuit. Mice become unable to identify the context as the correct predictor of the threat and show fear responses to a discrete cue not predicting the threat in normal conditions. These data demonstrate PTSD-like memory impairments in rodents and identify a potential pathophysiological mechanism of this condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaouane, Nadia -- Porte, Yves -- Vallee, Monique -- Brayda-Bruno, Laurent -- Mons, Nicole -- Calandreau, Ludovic -- Marighetto, Aline -- Piazza, Pier Vincenzo -- Desmedt, Aline -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1510-3. doi: 10.1126/science.1207615. Epub 2012 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR 5228, Centre de Neurosciences Integratives et Cognitives, Talence, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22362879" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiopathology ; Animals ; Conditioning (Psychology) ; Corticosterone/*administration & dosage/blood/metabolism/pharmacology ; Cues ; Electroshock ; *Fear ; Hippocampus/*physiopathology ; Male ; Memory Disorders/chemically induced/*physiopathology ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-fos/metabolism ; Restraint, Physical ; Stress Disorders, Post-Traumatic/*physiopathology ; Stress, Psychological
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    Microbial exposure during early life has persistent effects on natural killer T cell function (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-24
    Description: Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal-but not adult-GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437652/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olszak, Torsten -- An, Dingding -- Zeissig, Sebastian -- Vera, Miguel Pinilla -- Richter, Julia -- Franke, Andre -- Glickman, Jonathan N -- Siebert, Reiner -- Baron, Rebecca M -- Kasper, Dennis L -- Blumberg, Richard S -- AI090102/AI/NIAID NIH HHS/ -- DK034854/DK/NIDDK NIH HHS/ -- DK44319/DK/NIDDK NIH HHS/ -- DK51362/DK/NIDDK NIH HHS/ -- DK53056/DK/NIDDK NIH HHS/ -- DK88199/DK/NIDDK NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- R01 DK044319/DK/NIDDK NIH HHS/ -- R01 DK088199/DK/NIDDK NIH HHS/ -- R37 DK044319/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):489-93. doi: 10.1126/science.1219328. Epub 2012 Mar 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442383" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Antigens, CD1d/immunology ; Asthma/*immunology ; Bacteria/*growth & development ; Chemokine CXCL6/genetics/metabolism ; Colitis, Ulcerative/chemically induced/*immunology ; Colon/immunology/microbiology ; DNA Methylation ; Disease Models, Animal ; Disease Susceptibility ; Germ-Free Life ; Intestinal Mucosa/*immunology ; Intestines/immunology/*microbiology ; Lung/*immunology ; Mice ; Mice, Inbred C57BL ; Natural Killer T-Cells/*immunology ; Oxazolone ; Receptors, CXCR/genetics/metabolism ; Specific Pathogen-Free Organisms
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    Extrachromosomal microDNAs and chromosomal microdeletions in normal tissues (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-10
    Description: We have identified tens of thousands of short extrachromosomal circular DNAs (microDNA) in mouse tissues as well as mouse and human cell lines. These microDNAs are 200 to 400 base pairs long, are derived from unique nonrepetitive sequence, and are enriched in the 5'-untranslated regions of genes, exons, and CpG islands. Chromosomal loci that are enriched sources of microDNA in the adult brain are somatically mosaic for microdeletions that appear to arise from the excision of microDNAs. Germline microdeletions identified by the "Thousand Genomes" project may also arise from the excision of microDNAs in the germline lineage. We have thus identified a previously unknown DNA entity in mammalian cells and provide evidence that their generation leaves behind deletions in different genomic loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3703515/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3703515/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, Yoshiyuki -- Kumar, Pankaj -- Layer, Ryan -- Willcox, Smaranda -- Gagan, Jeffrey R -- Griffith, Jack D -- Dutta, Anindya -- ES013773/ES/NIEHS NIH HHS/ -- GM31819/GM/NIGMS NIH HHS/ -- GM84465/GM/NIGMS NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- R01 CA060499/CA/NCI NIH HHS/ -- R01 CA060499-18/CA/NCI NIH HHS/ -- R01 CA60499/CA/NCI NIH HHS/ -- R01 ES013773/ES/NIEHS NIH HHS/ -- R01 GM031819/GM/NIGMS NIH HHS/ -- R01 GM084465/GM/NIGMS NIH HHS/ -- R01 GM084465-04/GM/NIGMS NIH HHS/ -- T32 GM008136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):82-6. doi: 10.1126/science.1213307. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403181" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Animals ; Base Pairing ; Base Sequence ; Brain/*embryology ; Brain Chemistry ; Cell Line ; Cell Line, Tumor ; *Chromosome Deletion ; Chromosomes, Human/*genetics ; Chromosomes, Mammalian/*genetics ; CpG Islands ; DNA Replication ; *DNA, Circular/analysis/chemistry/isolation & purification/metabolism ; Exons ; Germ Cells/chemistry ; Heart/embryology ; Humans ; Liver/chemistry/embryology ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Molecular Sequence Data ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
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    Unique processing during a period of high excitation/inhibition balance in adult-born neurons (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-28
    Description: The adult dentate gyrus generates new granule cells (GCs) that develop over several weeks and integrate into the preexisting network. Although adult hippocampal neurogenesis has been implicated in learning and memory, the specific role of new GCs remains unclear. We examined whether immature adult-born neurons contribute to information encoding. By combining calcium imaging and electrophysiology in acute slices, we found that weak afferent activity recruits few mature GCs while activating a substantial proportion of the immature neurons. These different activation thresholds are dictated by an enhanced excitation/inhibition balance transiently expressed in immature GCs. Immature GCs exhibit low input specificity that switches with time toward a highly specific responsiveness. Therefore, activity patterns entering the dentate gyrus can undergo differential decoding by a heterogeneous population of GCs originated at different times.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385415/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385415/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marin-Burgin, Antonia -- Mongiat, Lucas A -- Pardi, M Belen -- Schinder, Alejandro F -- 55005963/Howard Hughes Medical Institute/ -- R03 TW008607/TW/FIC NIH HHS/ -- R03TW008607-01/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 9;335(6073):1238-42. doi: 10.1126/science.1214956. Epub 2012 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratorio de Plasticidad Neuronal, Instituto Leloir, Instituto de Investigaciones Bioquimicas de Buenos Aires-Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Avenida Patricias Argentinas 435, 1405 Buenos Aires, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dentate Gyrus/*cytology/*physiology ; Electric Stimulation ; Entorhinal Cortex/cytology/physiology ; Excitatory Postsynaptic Potentials ; Female ; GABAergic Neurons/physiology ; Glutamic Acid/metabolism ; Inhibitory Postsynaptic Potentials ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; *Neurogenesis ; Neuronal Plasticity ; Neurons/cytology/*physiology ; Patch-Clamp Techniques ; Perforant Pathway ; Synapses/physiology ; *Synaptic Potentials
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Germ cell migration across Sertoli cell tight junctions (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-22
    Description: The blood-testis barrier includes strands of tight junctions between somatic Sertoli cells that restricts solutes from crossing the paracellular space, creating a microenvironment within seminiferous tubules and providing immune privilege to meiotic and postmeiotic cells. Large cysts of germ cells transit the Sertoli cell tight junctions (SCTJs) without compromising their integrity. We used confocal microscopy to visualize SCTJ components during germ cell cyst migration across the SCTJs. Cysts become enclosed within a network of transient compartments fully bounded by old and new tight junctions. Dissolution of the old tight junctions releases the germ cells into the adluminal compartment, thus completing transit across the blood-testis barrier. Claudin 3, a tight junction protein, is transiently incorporated into new tight junctions and then replaced by claudin 11.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694388/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694388/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Benjamin E -- Braun, Robert E -- CA34196/CA/NCI NIH HHS/ -- HD12629/HD/NICHD NIH HHS/ -- P30 CA034196/CA/NCI NIH HHS/ -- U54 HD012629/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):798-802. doi: 10.1126/science.1219969. Epub 2012 Sep 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22997133" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Testis Barrier/*ultrastructure ; *Cell Movement ; Claudin-3/analysis/metabolism ; Claudins/analysis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Models, Biological ; Seminiferous Tubules/chemistry/ultrastructure ; Sertoli Cells/chemistry/physiology/*ultrastructure ; Spermatocytes/*physiology/ultrastructure ; Spermatogenesis ; Tight Junctions/chemistry/physiology/*ultrastructure
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A genomic regulatory element that directs assembly and function of immune-specific AP-1-IRF complexes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-18
    Description: Interferon regulatory factor 4 (IRF4) and IRF8 regulate B, T, macrophage, and dendritic cell differentiation. They are recruited to cis-regulatory Ets-IRF composite elements by PU.1 or Spi-B. How these IRFs target genes in most T cells is enigmatic given the absence of specific Ets partners. Chromatin immunoprecipitation sequencing in T helper 17 (T(H)17) cells reveals that IRF4 targets sequences enriched for activating protein 1 (AP-1)-IRF composite elements (AICEs) that are co-bound by BATF, an AP-1 factor required for T(H)17, B, and dendritic cell differentiation. IRF4 and BATF bind cooperatively to structurally divergent AICEs to promote gene activation and T(H)17 differentiation. The AICE motif directs assembly of IRF4 or IRF8 with BATF heterodimers and is also used in T(H)2, B, and dendritic cells. This genomic regulatory element and cognate factors appear to have evolved to integrate diverse immunomodulatory signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glasmacher, Elke -- Agrawal, Smita -- Chang, Abraham B -- Murphy, Theresa L -- Zeng, Wenwen -- Vander Lugt, Bryan -- Khan, Aly A -- Ciofani, Maria -- Spooner, Chauncey J -- Rutz, Sascha -- Hackney, Jason -- Nurieva, Roza -- Escalante, Carlos R -- Ouyang, Wenjun -- Littman, Dan R -- Murphy, Kenneth M -- Singh, Harinder -- RC1 AI087266/AI/NIAID NIH HHS/ -- RC4 AI092765/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):975-80. doi: 10.1126/science.1228309. Epub 2012 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Discovery Immunology, Genentech, Incorporated, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22983707" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation/genetics ; Chromatin Immunoprecipitation ; Humans ; Immunomodulation/*genetics ; Interferon Regulatory Factors/*metabolism ; Mice ; Mice, Inbred C57BL ; *Regulatory Elements, Transcriptional ; Th17 Cells/*immunology ; Transcription Factor AP-1/*metabolism ; *Transcriptional Activation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Leucine-tRNA initiates at CUG start codons for protein synthesis and presentation by MHC class I (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Effective immune surveillance by cytotoxic T cells requires newly synthesized polypeptides for presentation by major histocompatibility complex (MHC) class I molecules. These polypeptides are produced not only from conventional AUG-initiated, but also from cryptic non-AUG-initiated, reading frames by distinct translational mechanisms. Biochemical analysis of ribosomal initiation complexes at CUG versus AUG initiation codons revealed that cells use an elongator leucine-bound transfer RNA (Leu-tRNA) to initiate translation at cryptic CUG start codons. CUG/Leu-tRNA initiation was independent of the canonical initiator tRNA (AUG/Met-tRNA(i)(Met)) pathway but required expression of eukaryotic initiation factor 2A. Thus, a tRNA-based translation initiation mechanism allows non-AUG-initiated protein synthesis and supplies peptides for presentation by MHC class I molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Starck, Shelley R -- Jiang, Vivian -- Pavon-Eternod, Mariana -- Prasad, Sharanya -- McCarthy, Brian -- Pan, Tao -- Shastri, Nilabh -- New York, N.Y. -- Science. 2012 Jun 29;336(6089):1719-23. doi: 10.1126/science.1220270.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation/*genetics ; Antigen-Presenting Cells/immunology ; COS Cells ; Cercopithecus aethiops ; *Codon, Initiator ; HeLa Cells ; Histocompatibility Antigens Class I/*genetics/*immunology ; Humans ; Hybridomas/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Peptide Chain Initiation, Translational ; Protein Biosynthesis/*genetics ; *RNA, Transfer, Leu ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-11
    Description: Alzheimer's disease (AD) is associated with impaired clearance of beta-amyloid (Abeta) from the brain, a process normally facilitated by apolipoprotein E (apoE). ApoE expression is transcriptionally induced through the action of the nuclear receptors peroxisome proliferator-activated receptor gamma and liver X receptors in coordination with retinoid X receptors (RXRs). Oral administration of the RXR agonist bexarotene to a mouse model of AD resulted in enhanced clearance of soluble Abeta within hours in an apoE-dependent manner. Abeta plaque area was reduced more than 50% within just 72 hours. Furthermore, bexarotene stimulated the rapid reversal of cognitive, social, and olfactory deficits and improved neural circuit function. Thus, RXR activation stimulates physiological Abeta clearance mechanisms, resulting in the rapid reversal of a broad range of Abeta-induced deficits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651582/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651582/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cramer, Paige E -- Cirrito, John R -- Wesson, Daniel W -- Lee, C Y Daniel -- Karlo, J Colleen -- Zinn, Adriana E -- Casali, Brad T -- Restivo, Jessica L -- Goebel, Whitney D -- James, Michael J -- Brunden, Kurt R -- Wilson, Donald A -- Landreth, Gary E -- AG030482-03S1/AG/NIA NIH HHS/ -- DC003906/DC/NIDCD NIH HHS/ -- K01 AG029524/AG/NIA NIH HHS/ -- P50-AG005681/AG/NIA NIH HHS/ -- R01 AG030482/AG/NIA NIH HHS/ -- R01 AG037693/AG/NIA NIH HHS/ -- R01 DC003906/DC/NIDCD NIH HHS/ -- R01-AG037693/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1503-6. doi: 10.1126/science.1217697. Epub 2012 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323736" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy/*metabolism ; Amyloid beta-Peptides/*metabolism ; Amyloidosis/drug therapy/metabolism ; Animals ; Apolipoproteins E/*metabolism ; Astrocytes/drug effects/metabolism ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Disease Models, Animal ; Extracellular Fluid/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/drug effects/metabolism ; Molecular Targeted Therapy ; Odors ; Olfactory Pathways/drug effects/physiology ; Orphan Nuclear Receptors/metabolism ; PPAR gamma/metabolism ; Phagocytosis ; Plaque, Amyloid/drug therapy ; Retinoid X Receptors/agonists/metabolism ; Tetrahydronaphthalenes/*pharmacology/*therapeutic use
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    Transcriptional architecture and chromatin landscape of the core circadian clock in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: The mammalian circadian clock involves a transcriptional feed back loop in which CLOCK and BMAL1 activate the Period and Cryptochrome genes, which then feedback and repress their own transcription. We have interrogated the transcriptional architecture of the circadian transcriptional regulatory loop on a genome scale in mouse liver and find a stereotyped, time-dependent pattern of transcription factor binding, RNA polymerase II (RNAPII) recruitment, RNA expression, and chromatin states. We find that the circadian transcriptional cycle of the clock consists of three distinct phases: a poised state, a coordinated de novo transcriptional activation state, and a repressed state. Only 22% of messenger RNA (mRNA) cycling genes are driven by de novo transcription, suggesting that both transcriptional and posttranscriptional mechanisms underlie the mammalian circadian clock. We also find that circadian modulation of RNAPII recruitment and chromatin remodeling occurs on a genome-wide scale far greater than that seen previously by gene expression profiling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koike, Nobuya -- Yoo, Seung-Hee -- Huang, Hung-Chung -- Kumar, Vivek -- Lee, Choogon -- Kim, Tae-Kyung -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- R01 NS053616/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):349-54. doi: 10.1126/science.1226339. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936566" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Chromatin/*metabolism ; Chromatin Assembly and Disassembly/genetics ; Circadian Clocks/*genetics ; Cryptochromes/*genetics ; DNA, Intergenic ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; Gene Expression Profiling ; Genetic Loci ; Histones/metabolism ; Liver/metabolism/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Period Circadian Proteins/genetics ; RNA Polymerase II/metabolism ; RNA, Messenger/genetics ; *Transcription, Genetic ; *Transcriptional Activation
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    Shear-activated nanotherapeutics for drug targeting to obstructed blood vessels (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-07
    Description: Obstruction of critical blood vessels due to thrombosis or embolism is a leading cause of death worldwide. Here, we describe a biomimetic strategy that uses high shear stress caused by vascular narrowing as a targeting mechanism--in the same way platelets do--to deliver drugs to obstructed blood vessels. Microscale aggregates of nanoparticles were fabricated to break up into nanoscale components when exposed to abnormally high fluid shear stress. When coated with tissue plasminogen activator and administered intravenously in mice, these shear-activated nanotherapeutics induce rapid clot dissolution in a mesenteric injury model, restore normal flow dynamics, and increase survival in an otherwise fatal mouse pulmonary embolism model. This biophysical strategy for drug targeting, which lowers required doses and minimizes side effects while maximizing drug efficacy, offers a potential new approach for treatment of life-threatening diseases that result from acute vascular occlusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korin, Netanel -- Kanapathipillai, Mathumai -- Matthews, Benjamin D -- Crescente, Marilena -- Brill, Alexander -- Mammoto, Tadanori -- Ghosh, Kaustabh -- Jurek, Samuel -- Bencherif, Sidi A -- Bhatta, Deen -- Coskun, Ahmet U -- Feldman, Charles L -- Wagner, Denisa D -- Ingber, Donald E -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):738-42. doi: 10.1126/science.1217815. Epub 2012 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22767894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomimetic Materials ; Blood Circulation ; Drug Delivery Systems/*methods ; Fibrinolytic Agents/*administration & dosage ; Hemodynamics ; Hemorheology ; Lactic Acid ; Male ; Mesenteric Arteries ; Mesenteric Vascular Occlusion/*drug therapy ; Mice ; Mice, Inbred C57BL ; Microfluidic Analytical Techniques ; Models, Anatomic ; *Nanoparticles ; Polyglycolic Acid ; Pulmonary Embolism/*drug therapy ; Stress, Mechanical ; Thrombosis/*drug therapy/prevention & control ; Tissue Plasminogen Activator/*administration & dosage
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    B cells use mechanical energy to discriminate antigen affinities (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-21
    Description: The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natkanski, Elizabeth -- Lee, Wing-Yiu -- Mistry, Bhakti -- Casal, Antonio -- Molloy, Justin E -- Tolar, Pavel -- MC_U117570592/Medical Research Council/United Kingdom -- MC_U117597138/Medical Research Council/United Kingdom -- U117570592/Medical Research Council/United Kingdom -- U117597138/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1587-90. doi: 10.1126/science.1237572. Epub 2013 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23686338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; *Antigen Presentation ; Antigens/*immunology ; B-Lymphocytes/*immunology ; Cells, Cultured ; Mechanical Processes ; Mice ; Mice, Inbred C57BL ; Microscopy, Atomic Force ; Nonmuscle Myosin Type IIA/*physiology ; Receptors, Antigen, B-Cell/immunology
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    Role of tissue protection in lethal respiratory viral-bacterial coinfection (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-27
    Description: Secondary bacterial pneumonia leads to increased morbidity and mortality from influenza virus infections. What causes this increased susceptibility, however, is not well defined. Host defense from infection relies not only on immune resistance mechanisms but also on the ability to tolerate a given level of pathogen burden. Failure of either resistance or tolerance can contribute to disease severity, making it hard to distinguish their relative contribution. We employ a coinfection mouse model of influenza virus and Legionella pneumophila in which we can separate resistance and tolerance. We demonstrate that influenza virus can promote susceptibility to lethal bacterial coinfection, even when bacterial infection is controlled by the immune system. We propose that this failure of host defense is due to impaired ability to tolerate tissue damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933032/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jamieson, Amanda M -- Pasman, Lesley -- Yu, Shuang -- Gamradt, Pia -- Homer, Robert J -- Decker, Thomas -- Medzhitov, Ruslan -- AI R01 055502/AI/NIAID NIH HHS/ -- R01 046688/PHS HHS/ -- R01 AI046688/AI/NIAID NIH HHS/ -- R01 AI055502/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Jun 7;340(6137):1230-4. doi: 10.1126/science.1233632. Epub 2013 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. amanda_jamieson@brown.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23618765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1 ; Coinfection/*immunology/pathology ; Disease Models, Animal ; Host-Pathogen Interactions/immunology ; Interleukin-1beta/metabolism ; *Legionella pneumophila ; Legionnaires' Disease/*immunology/pathology ; Lung/microbiology/pathology/virology ; Mice ; Mice, Inbred C57BL ; *Orthomyxoviridae ; Orthomyxoviridae Infections/*immunology/pathology ; Pneumonia, Bacterial/*immunology/pathology ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Global epigenomic reconfiguration during mammalian brain development (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-06
    Description: DNA methylation is implicated in mammalian brain development and plasticity underlying learning and memory. We report the genome-wide composition, patterning, cell specificity, and dynamics of DNA methylation at single-base resolution in human and mouse frontal cortex throughout their lifespan. Widespread methylome reconfiguration occurs during fetal to young adult development, coincident with synaptogenesis. During this period, highly conserved non-CG methylation (mCH) accumulates in neurons, but not glia, to become the dominant form of methylation in the human neuronal genome. Moreover, we found an mCH signature that identifies genes escaping X-chromosome inactivation. Last, whole-genome single-base resolution 5-hydroxymethylcytosine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions that are CG-demethylated and activated in the adult brain and that CG demethylation at these hmC-poised loci depends on Tet2 activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785061/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785061/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lister, Ryan -- Mukamel, Eran A -- Nery, Joseph R -- Urich, Mark -- Puddifoot, Clare A -- Johnson, Nicholas D -- Lucero, Jacinta -- Huang, Yun -- Dwork, Andrew J -- Schultz, Matthew D -- Yu, Miao -- Tonti-Filippini, Julian -- Heyn, Holger -- Hu, Shijun -- Wu, Joseph C -- Rao, Anjana -- Esteller, Manel -- He, Chuan -- Haghighi, Fatemeh G -- Sejnowski, Terrence J -- Behrens, M Margarita -- Ecker, Joseph R -- AI44432/AI/NIAID NIH HHS/ -- CA151535/CA/NCI NIH HHS/ -- HD065812/HD/NICHD NIH HHS/ -- HG006827/HG/NHGRI NIH HHS/ -- K99NS080911/NS/NINDS NIH HHS/ -- MH094670/MH/NIMH NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 CA151535/CA/NCI NIH HHS/ -- R01 HD065812/HD/NICHD NIH HHS/ -- R01 HG006827/HG/NHGRI NIH HHS/ -- R01 MH094670/MH/NIMH NIH HHS/ -- R01 MH094774/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):1237905. doi: 10.1126/science.1237905. Epub 2013 Jul 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. ryan.lister@uwa.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828890" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Adult ; Animals ; Base Sequence ; Conserved Sequence ; Cytosine/*analogs & derivatives/metabolism ; *DNA Methylation ; *Epigenesis, Genetic ; Epigenomics ; Frontal Lobe/*growth & development ; *Gene Expression Regulation, Developmental ; Genome-Wide Association Study ; Humans ; Longevity ; Mice ; Mice, Inbred C57BL ; X Chromosome Inactivation/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Caspase-11 protects against bacteria that escape the vacuole (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-26
    Description: Caspases are either apoptotic or inflammatory. Among inflammatory caspases, caspase-1 and -11 trigger pyroptosis, a form of programmed cell death. Whereas both can be detrimental in inflammatory disease, only caspase-1 has an established protective role during infection. Here, we report that caspase-11 is required for innate immunity to cytosolic, but not vacuolar, bacteria. Although Salmonella typhimurium and Legionella pneumophila normally reside in the vacuole, specific mutants (sifA and sdhA, respectively) aberrantly enter the cytosol. These mutants triggered caspase-11, which enhanced clearance of S. typhimurium sifA in vivo. This response did not require NLRP3, NLRC4, or ASC inflammasome pathways. Burkholderia species that naturally invade the cytosol also triggered caspase-11, which protected mice from lethal challenge with B. thailandensis and B. pseudomallei. Thus, caspase-11 is critical for surviving exposure to ubiquitous environmental pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697099/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3697099/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aachoui, Youssef -- Leaf, Irina A -- Hagar, Jon A -- Fontana, Mary F -- Campos, Cristine G -- Zak, Daniel E -- Tan, Michael H -- Cotter, Peggy A -- Vance, Russell E -- Aderem, Alan -- Miao, Edward A -- AI057141/AI/NIAID NIH HHS/ -- AI063302/AI/NIAID NIH HHS/ -- AI065359/AI/NIAID NIH HHS/ -- AI075039/AI/NIAID NIH HHS/ -- AI080749/AI/NIAID NIH HHS/ -- AI097518/AI/NIAID NIH HHS/ -- P01 AI063302/AI/NIAID NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- R01 AI075039/AI/NIAID NIH HHS/ -- R01 AI080749/AI/NIAID NIH HHS/ -- R01 AI097518/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 AI057141/AI/NIAID NIH HHS/ -- U54 AI065359/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):975-8. doi: 10.1126/science.1230751. Epub 2013 Jan 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23348507" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkholderia/pathogenicity/physiology ; Burkholderia Infections/enzymology/immunology/metabolism ; Burkholderia pseudomallei/pathogenicity/physiology ; Caspases/*metabolism ; *Cell Death ; Cytosol/*microbiology ; Gram-Negative Bacterial Infections/enzymology/*immunology/microbiology ; Immunity, Innate ; Inflammasomes/metabolism ; Macrophages/immunology/*microbiology ; Mice ; Mice, Inbred C57BL ; Phagosomes/microbiology ; Salmonella Infections, Animal/enzymology/immunology/microbiology ; Salmonella typhimurium/pathogenicity/physiology ; Vacuoles/*microbiology
    Print ISSN: 0036-8075
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    Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-02
    Description: Prenatal infection and exposure to traumatizing experiences during peripuberty have each been associated with increased risk for neuropsychiatric disorders. Evidence is lacking for the cumulative impact of such prenatal and postnatal environmental challenges on brain functions and vulnerability to psychiatric disease. Here, we show in a translational mouse model that combined exposure to prenatal immune challenge and peripubertal stress induces synergistic pathological effects on adult behavioral functions and neurochemistry. We further demonstrate that the prenatal insult markedly increases the vulnerability of the pubescent offspring to brain immune changes in response to stress. Our findings reveal interactions between two adverse environmental factors that have individually been associated with neuropsychiatric disease and support theories that mental illnesses with delayed onsets involve multiple environmental hits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giovanoli, Sandra -- Engler, Harald -- Engler, Andrea -- Richetto, Juliet -- Voget, Mareike -- Willi, Roman -- Winter, Christine -- Riva, Marco A -- Mortensen, Preben B -- Feldon, Joram -- Schedlowski, Manfred -- Meyer, Urs -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1095-9. doi: 10.1126/science.1228261.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiology and Behavior Laboratory, Swiss Federal Institute of Technology (ETH) Zurich, 8603 Schwerzenbach, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/immunology ; Disease Models, Animal ; Female ; Humans ; Mental Disorders/*immunology ; Mice ; Mice, Inbred C57BL ; Poly I-C/immunology/pharmacology ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology/virology ; Puberty/*immunology ; Stress, Physiological/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interstitial dendritic cell guidance by haptotactic chemokine gradients (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-01-19
    Description: Directional guidance of cells via gradients of chemokines is considered crucial for embryonic development, cancer dissemination, and immune responses. Nevertheless, the concept still lacks direct experimental confirmation in vivo. Here, we identify endogenous gradients of the chemokine CCL21 within mouse skin and show that they guide dendritic cells toward lymphatic vessels. Quantitative imaging reveals depots of CCL21 within lymphatic endothelial cells and steeply decaying gradients within the perilymphatic interstitium. These gradients match the migratory patterns of the dendritic cells, which directionally approach vessels from a distance of up to 90-micrometers. Interstitial CCL21 is immobilized to heparan sulfates, and its experimental delocalization or swamping the endogenous gradients abolishes directed migration. These findings functionally establish the concept of haptotaxis, directed migration along immobilized gradients, in tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, Michele -- Hauschild, Robert -- Schwarz, Jan -- Moussion, Christine -- de Vries, Ingrid -- Legler, Daniel F -- Luther, Sanjiv A -- Bollenbach, Tobias -- Sixt, Michael -- New York, N.Y. -- Science. 2013 Jan 18;339(6117):328-32. doi: 10.1126/science.1228456.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IST Austria (Institute of Science and Technology Austria), Klosterneuburg, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23329049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokine CCL19/metabolism ; Chemokine CCL21/chemistry/*immunology ; Chemotaxis/*immunology ; Dendritic Cells/*immunology ; Heparitin Sulfate/chemistry ; Immobilized Proteins/chemistry/immunology ; Lymphatic Vessels/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Receptors, CCR7/genetics ; Skin/*immunology
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    Suppression of oxidative stress by beta-hydroxybutyrate, an endogenous histone deacetylase inhibitor (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-12
    Description: Concentrations of acetyl-coenzyme A and nicotinamide adenine dinucleotide (NAD(+)) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body d-beta-hydroxybutyrate (betaOHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous betaOHB, or fasting or calorie restriction, two conditions associated with increased betaOHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by betaOHB was correlated with global changes in transcription, including that of the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with betaOHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with betaOHB conferred substantial protection against oxidative stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimazu, Tadahiro -- Hirschey, Matthew D -- Newman, John -- He, Wenjuan -- Shirakawa, Kotaro -- Le Moan, Natacha -- Grueter, Carrie A -- Lim, Hyungwook -- Saunders, Laura R -- Stevens, Robert D -- Newgard, Christopher B -- Farese, Robert V Jr -- de Cabo, Rafael -- Ulrich, Scott -- Akassoglou, Katerina -- Verdin, Eric -- P30 DK026743/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 DK056084/DK/NIDDK NIH HHS/ -- T32 AG000212/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2013 Jan 11;339(6116):211-4. doi: 10.1126/science.1227166. Epub 2012 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23223453" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxybutyric Acid/blood/*metabolism/pharmacology ; Acetylation ; Animals ; Caloric Restriction ; Catalase/metabolism ; Fasting ; Forkhead Transcription Factors/genetics ; HEK293 Cells ; Histone Deacetylase Inhibitors/blood/*metabolism/pharmacology ; Histone Deacetylases/genetics/*metabolism ; Histones/metabolism ; Humans ; Kidney/drug effects/*metabolism ; Lipid Peroxidation ; Metallothionein/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; *Oxidative Stress/genetics ; Promoter Regions, Genetic ; RNA, Small Interfering ; Superoxide Dismutase/metabolism ; Transcription, Genetic ; Transcriptional Activation
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    Compartmentalization of GABAergic inhibition by dendritic spines (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-11
    Description: gamma-aminobutyric acid-mediated (GABAergic) inhibition plays a critical role in shaping neuronal activity in the neocortex. Numerous experimental investigations have examined perisomatic inhibitory synapses, which control action potential output from pyramidal neurons. However, most inhibitory synapses in the neocortex are formed onto pyramidal cell dendrites, where theoretical studies suggest they may focally regulate cellular activity. The precision of GABAergic control over dendritic electrical and biochemical signaling is unknown. By using cell type-specific optical stimulation in combination with two-photon calcium (Ca(2+)) imaging, we show that somatostatin-expressing interneurons exert compartmentalized control over postsynaptic Ca(2+) signals within individual dendritic spines. This highly focal inhibitory action is mediated by a subset of GABAergic synapses that directly target spine heads. GABAergic inhibition thus participates in localized control of dendritic electrical and biochemical signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752161/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752161/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiu, Chiayu Q -- Lur, Gyorgy -- Morse, Thomas M -- Carnevale, Nicholas T -- Ellis-Davies, Graham C R -- Higley, Michael J -- DC009977/DC/NIDCD NIH HHS/ -- GM053395/GM/NIGMS NIH HHS/ -- K01 MH097961/MH/NIMH NIH HHS/ -- MH099045/MH/NIMH NIH HHS/ -- NS011613/NS/NINDS NIH HHS/ -- NS069720/NS/NINDS NIH HHS/ -- R01 DC009977/DC/NIDCD NIH HHS/ -- R01 GM053395/GM/NIGMS NIH HHS/ -- R01 MH099045/MH/NIMH NIH HHS/ -- R01 NS011613/NS/NINDS NIH HHS/ -- R01 NS069720/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 10;340(6133):759-62. doi: 10.1126/science.1234274.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Computer Simulation ; Dendritic Spines/*physiology ; Female ; Glutamic Acid/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neocortex/*physiology ; *Neural Inhibition ; Photic Stimulation ; Pyramidal Cells/*physiology ; Rhodopsin/metabolism ; Synapses/physiology ; gamma-Aminobutyric Acid/*physiology
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    Interferon-epsilon protects the female reproductive tract from viral and bacterial infection (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-03-02
    Description: The innate immune system senses pathogens through pattern-recognition receptors (PRRs) that signal to induce effector cytokines, such as type I interferons (IFNs). We characterized IFN-epsilon as a type I IFN because it signaled via the Ifnar1 and Ifnar2 receptors to induce IFN-regulated genes. In contrast to other type I IFNs, IFN-epsilon was not induced by known PRR pathways; instead, IFN-epsilon was constitutively expressed by epithelial cells of the female reproductive tract (FRT) and was hormonally regulated. Ifn-epsilon-deficient mice had increased susceptibility to infection of the FRT by the common sexually transmitted infections (STIs) herpes simplex virus 2 and Chlamydia muridarum. Thus, IFN-epsilon is a potent antipathogen and immunoregulatory cytokine that may be important in combating STIs that represent a major global health and socioeconomic burden.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617553/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617553/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fung, Ka Yee -- Mangan, Niamh E -- Cumming, Helen -- Horvat, Jay C -- Mayall, Jemma R -- Stifter, Sebastian A -- De Weerd, Nicole -- Roisman, Laila C -- Rossjohn, Jamie -- Robertson, Sarah A -- Schjenken, John E -- Parker, Belinda -- Gargett, Caroline E -- Nguyen, Hong P T -- Carr, Daniel J -- Hansbro, Philip M -- Hertzog, Paul J -- R01 AI053108/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1088-92. doi: 10.1126/science.1233321.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chlamydia Infections/genetics/*immunology ; *Chlamydia muridarum ; Estrogens/administration & dosage/immunology ; Female ; HEK293 Cells ; Herpes Genitalis/genetics/*immunology ; *Herpesvirus 2, Human ; Humans ; Interferons/genetics/*immunology ; Ligands ; Mice ; Mice, Inbred C57BL ; Oligodeoxyribonucleotides/immunology ; Poly I-C/immunology ; Poly dA-dT/immunology ; Toll-Like Receptors/*immunology ; Uterus/immunology ; Vagina/*immunology/microbiology/virology
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    Gut microbiomes of Malawian twin pairs discordant for kwashiorkor (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-02-01
    Description: Kwashiorkor, an enigmatic form of severe acute malnutrition, is the consequence of inadequate nutrient intake plus additional environmental insults. To investigate the role of the gut microbiome, we studied 317 Malawian twin pairs during the first 3 years of life. During this time, half of the twin pairs remained well nourished, whereas 43% became discordant, and 7% manifested concordance for acute malnutrition. Both children in twin pairs discordant for kwashiorkor were treated with a peanut-based, ready-to-use therapeutic food (RUTF). Time-series metagenomic studies revealed that RUTF produced a transient maturation of metabolic functions in kwashiorkor gut microbiomes that regressed when administration of RUTF was stopped. Previously frozen fecal communities from several discordant pairs were each transplanted into gnotobiotic mice. The combination of Malawian diet and kwashiorkor microbiome produced marked weight loss in recipient mice, accompanied by perturbations in amino acid, carbohydrate, and intermediary metabolism that were only transiently ameliorated with RUTF. These findings implicate the gut microbiome as a causal factor in kwashiorkor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667500/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Michelle I -- Yatsunenko, Tanya -- Manary, Mark J -- Trehan, Indi -- Mkakosya, Rajhab -- Cheng, Jiye -- Kau, Andrew L -- Rich, Stephen S -- Concannon, Patrick -- Mychaleckyj, Josyf C -- Liu, Jie -- Houpt, Eric -- Li, Jia V -- Holmes, Elaine -- Nicholson, Jeremy -- Knights, Dan -- Ursell, Luke K -- Knight, Rob -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- DK30292/DK/NIDDK NIH HHS/ -- F32 DK091044/DK/NIDDK NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- T32 HD049338/HD/NICHD NIH HHS/ -- T32-HD049338/HD/NICHD NIH HHS/ -- T35 DK074375/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 1;339(6119):548-54. doi: 10.1126/science.1229000. Epub 2013 Jan 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University in St. Louis, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23363771" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; Arachis ; Carbohydrate Metabolism ; Child, Preschool ; Diseases in Twins/*microbiology ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Infant ; Kwashiorkor/diet therapy/epidemiology/*microbiology ; Longitudinal Studies ; Malawi/epidemiology ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Fear learning enhances neural responses to threat-predictive sensory stimuli (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: The central nervous system rapidly learns that particular stimuli predict imminent danger. This learning is thought to involve associations between neutral and harmful stimuli in cortical and limbic brain regions, though associative neuroplasticity in sensory structures is increasingly appreciated. We observed the synaptic output of olfactory sensory neurons (OSNs) in individual mice before and after they learned that a particular odor indicated an impending foot shock. OSNs are the first cells in the olfactory system, physically contacting the odor molecules in the nose and projecting their axons to the brain's olfactory bulb. OSN output evoked by the shock-predictive odor was selectively facilitated after fear conditioning. These results indicate that affective information about a stimulus can be encoded in its very earliest representation in the nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011636/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011636/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kass, Marley D -- Rosenthal, Michelle C -- Pottackal, Joseph -- McGann, John P -- DC009442/DC/NIDCD NIH HHS/ -- DC013090/DC/NIDCD NIH HHS/ -- MH101293/MH/NIMH NIH HHS/ -- R00 DC009442/DC/NIDCD NIH HHS/ -- R01 DC013090/DC/NIDCD NIH HHS/ -- R01 MH101293/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1389-92. doi: 10.1126/science.1244916.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Behavioral and Systems Neuroscience Section, Department of Psychology, Rutgers, The State University of New Jersey, 152 Frelinghuysen Road, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical/physiology ; Fear/*psychology ; Learning/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity ; *Odors ; Olfactory Receptor Neurons/*physiology ; Smell/*physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Erythropoietin derived by chemical synthesis (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: Erythropoietin is a signaling glycoprotein that controls the fundamental process of erythropoiesis, orchestrating the production and maintenance of red blood cells. As administrated clinically, erythropoietin has a polypeptide backbone with complex dishomogeneity in its carbohydrate domains. Here we describe the total synthesis of homogeneous erythropoietin with consensus carbohydrate domains incorporated at all of the native glycosylation sites. The oligosaccharide sectors were built by total synthesis and attached stereospecifically to peptidyl fragments of the wild-type primary sequence, themselves obtained by solid-phase peptide synthesis. The glycopeptidyl constructs were joined by chemical ligation, followed by metal-free dethiylation, and subsequently folded. This homogeneous erythropoietin glycosylated at the three wild-type aspartates with N-linked high-mannose sialic acid-containing oligosaccharides and O-linked glycophorin exhibits Procrit-level in vivo activity in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ping -- Dong, Suwei -- Shieh, Jae-Hung -- Peguero, Elizabeth -- Hendrickson, Ronald -- Moore, Malcolm A S -- Danishefsky, Samuel J -- HL025848/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 GM109760/GM/NIGMS NIH HHS/ -- R01 HL025848/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1357-60. doi: 10.1126/science.1245095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Bioorganic Chemistry, Sloan-Kettering Institute for Cancer Research, 1275 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337294" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Cells, Cultured ; Consensus Sequence ; Dose-Response Relationship, Drug ; Erythrocyte Count ; Erythropoietin/*administration & dosage/*chemical synthesis/chemistry ; Glycophorin/chemistry ; Glycosylation ; Injections, Subcutaneous ; Mannose/chemistry ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; N-Acetylneuraminic Acid/chemistry ; Oligosaccharides/chemistry ; Reticulocytes/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Sleep drives metabolite clearance from the adult brain (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-19
    Description: The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of beta-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880190/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, Lulu -- Kang, Hongyi -- Xu, Qiwu -- Chen, Michael J -- Liao, Yonghong -- Thiyagarajan, Meenakshisundaram -- O'Donnell, John -- Christensen, Daniel J -- Nicholson, Charles -- Iliff, Jeffrey J -- Takano, Takahiro -- Deane, Rashid -- Nedergaard, Maiken -- NS028642/NS/NINDS NIH HHS/ -- NS078167/NS/NINDS NIH HHS/ -- NS078304/NS/NINDS NIH HHS/ -- R01 DE022743/DE/NIDCR NIH HHS/ -- R01 NS075177/NS/NINDS NIH HHS/ -- R01 NS078167/NS/NINDS NIH HHS/ -- R01 NS078304/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 18;342(6156):373-7. doi: 10.1126/science.1241224.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, Department of Neurosurgery, University of Rochester Medical Center, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24136970" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Antagonists/administration & dosage ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism/physiology ; Cerebral Cortex/metabolism/physiology ; Cerebrospinal Fluid/metabolism ; Diffusion ; Electroencephalography ; Extracellular Space ; Intracellular Space ; Male ; Mice ; Mice, Inbred C57BL ; Neurodegenerative Diseases/*metabolism ; Quaternary Ammonium Compounds/chemistry ; Receptors, Adrenergic/metabolism ; Sleep/*physiology ; Wakefulness/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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