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  • Mice, Inbred C57BL  (46)
  • American Association for the Advancement of Science (AAAS)  (46)
  • 2015-2019
  • 2010-2014  (46)
  • 2010  (46)
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  • 2015-2019
  • 2010-2014  (46)
Year
  • 1
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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
    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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    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
    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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    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
    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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    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
    Electronic ISSN: 1095-9203
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  • 5
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 6
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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
    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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  • 7
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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)
    Details
    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
    Print ISSN: 0036-8075
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  • 8
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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)
    Details
    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
    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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  • 9
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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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  • 10
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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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  • 11
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    Sex-specific parent-of-origin allelic expression in the mouse brain (2010)
    American Association for the Advancement of Science (AAAS)
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    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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  • 12
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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
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  • 13
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    Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture (2010)
    American Association for the Advancement of Science (AAAS)
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    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)
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    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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  • 15
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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
    Print ISSN: 0036-8075
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  • 17
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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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  • 18
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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
    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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  • 19
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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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  • 20
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    Cortical plasticity induced by inhibitory neuron transplantation (2010)
    American Association for the Advancement of Science (AAAS)
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    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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  • 21
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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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  • 22
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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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  • 23
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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
    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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    An early T cell lineage commitment checkpoint dependent on the transcription factor Bcl11b (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: The identities of the regulators that mediate commitment of hematopoietic precursors to the T lymphocyte lineage have been unknown. The last stage of T lineage commitment in vivo involves mechanisms to suppress natural killer cell potential, to suppress myeloid and dendritic cell potential, and to silence the stem cell or progenitor cell regulatory functions that initially provide T cell receptor-independent self-renewal capability. The zinc finger transcription factor Bcl11b is T cell-specific in expression among hematopoietic cell types and is first expressed in precursors immediately before T lineage commitment. We found that Bcl11b is necessary for T lineage commitment in mice and is specifically required both to repress natural killer cell-associated genes and to down-regulate a battery of stem cell or progenitor cell genes at the pivotal stage of commitment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935300/" 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/PMC2935300/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Long -- Leid, Mark -- Rothenberg, Ellen V -- F06 TW002367/TW/FIC NIH HHS/ -- F06 TW002367-01A1/TW/FIC NIH HHS/ -- R01 GM060852/GM/NIGMS NIH HHS/ -- R01 GM060852-04/GM/NIGMS NIH HHS/ -- R01 GM60852/GM/NIGMS NIH HHS/ -- R33 HL089123/HL/NHLBI NIH HHS/ -- R33 HL089123-03/HL/NHLBI NIH HHS/ -- RC2 CA148278/CA/NCI NIH HHS/ -- RC2 CA148278-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):89-93. doi: 10.1126/science.1188989.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Cells, Cultured ; Down-Regulation ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, T-Cell Receptor delta ; Genes, T-Cell Receptor gamma ; Killer Cells, Natural/cytology/physiology ; *Lymphopoiesis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Precursor Cells, T-Lymphoid/cytology/immunology/*physiology ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Receptors, Notch/metabolism ; Repressor Proteins/deficiency/genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/cytology/metabolism/*physiology ; Transcription Factors/genetics/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
    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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    Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" 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/PMC3628452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Burke, Shannon -- Wang, Juexuan -- Chen, Xiongfeng -- Ortiz, Mariaestela -- Lee, Song-Choon -- Lu, Dong -- Campos, Lia -- Goulding, David -- Ng, Bee Ling -- Dougan, Gordon -- Huntly, Brian -- Gottgens, Bertie -- Jenkins, Nancy A -- Copeland, Neal G -- Colucci, Francesco -- Liu, Pentao -- 076962/Wellcome Trust/United Kingdom -- 077186/Wellcome Trust/United Kingdom -- G0501150/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- G116/187/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):85-9. doi: 10.1126/science.1188063. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Cytotoxicity, Immunologic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, T-Cell Receptor beta ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Melanoma, Experimental/immunology/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Precursor Cells, T-Lymphoid/cytology/physiology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; Stromal Cells/cytology/physiology ; T-Lymphocytes/cytology/immunology/*physiology/transplantation ; Tamoxifen/analogs & derivatives/pharmacology ; Tumor Suppressor Proteins/*genetics/*metabolism
    Print ISSN: 0036-8075
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    Alleviating neuropathic pain hypersensitivity by inhibiting PKMzeta in the anterior cingulate cortex (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Synaptic plasticity is a key mechanism for chronic pain. It occurs at different levels of the central nervous system, including spinal cord and cortex. Studies have mainly focused on signaling proteins that trigger these plastic changes, whereas few have addressed the maintenance of plastic changes related to chronic pain. We found that protein kinase M zeta (PKMzeta) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC). Peripheral nerve injury caused activation of PKMzeta in the ACC, and inhibiting PKMzeta by a selective inhibitor, zeta-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation. Microinjection of ZIP into the ACC blocked behavioral sensitization. These results suggest that PKMzeta in the ACC acts to maintain neuropathic pain. PKMzeta could thus be a new therapeutic target for treating chronic pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Xiang-Yao -- Ko, Hyoung-Gon -- Chen, Tao -- Descalzi, Giannina -- Koga, Kohei -- Wang, Hansen -- Kim, Susan S -- Shang, Yuze -- Kwak, Chuljung -- Park, Soo-Won -- Shim, Jaehoon -- Lee, Kyungmin -- Collingridge, Graham L -- Kaang, Bong-Kiun -- Zhuo, Min -- CIHR66975/Canadian Institutes of Health Research/Canada -- CIHR84256/Canadian Institutes of Health Research/Canada -- G0601813/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1400-4. doi: 10.1126/science.1191792.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Faculty of Medicine, Center for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127255" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/metabolism ; Analgesics/administration & dosage/pharmacology ; Animals ; Enzyme Inhibitors/administration & dosage/*pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Gyrus Cinguli/*enzymology/physiology ; Long-Term Potentiation ; Male ; Memory/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuralgia/*drug therapy/*enzymology ; Patch-Clamp Techniques ; Peptides/administration & dosage/*pharmacology ; Peroneal Nerve/injuries ; Phosphorylation ; Protein Kinase C/*antagonists & inhibitors/*metabolism ; Receptors, AMPA/metabolism ; Sensory Receptor Cells/physiology ; Somatosensory Cortex/physiology ; Synapses/physiology ; Synaptic Transmission
    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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    MicroRNA-33 and the SREBP host genes cooperate to control cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Proper coordination of cholesterol biosynthesis and trafficking is essential to human health. The sterol regulatory element-binding proteins (SREBPs) are key transcription regulators of genes involved in cholesterol biosynthesis and uptake. We show here that microRNAs (miR-33a/b) embedded within introns of the SREBP genes target the adenosine triphosphate-binding cassette transporter A1 (ABCA1), an important regulator of high-density lipoprotein (HDL) synthesis and reverse cholesterol transport, for posttranscriptional repression. Antisense inhibition of miR-33 in mouse and human cell lines causes up-regulation of ABCA1 expression and increased cholesterol efflux, and injection of mice on a western-type diet with locked nucleic acid-antisense oligonucleotides results in elevated plasma HDL. Our findings indicate that miR-33 acts in concert with the SREBP host genes to control cholesterol homeostasis and suggest that miR-33 may represent a therapeutic target for ameliorating cardiometabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840500/" 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/PMC3840500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Najafi-Shoushtari, S Hani -- Kristo, Fjoralba -- Li, Yingxia -- Shioda, Toshi -- Cohen, David E -- Gerszten, Robert E -- Naar, Anders M -- P30 DK034854/DK/NIDDK NIH HHS/ -- P30 DK34854/DK/NIDDK NIH HHS/ -- R01 DK048873/DK/NIDDK NIH HHS/ -- R01 DK056626/DK/NIDDK NIH HHS/ -- R01 GM071449/GM/NIGMS NIH HHS/ -- R01DK48873/DK/NIDDK NIH HHS/ -- R01DK56626/DK/NIDDK NIH HHS/ -- R01GM071449/GM/NIGMS NIH HHS/ -- R21 DK084459/DK/NIDDK NIH HHS/ -- R21DK084459/DK/NIDDK NIH HHS/ -- R37 DK048873/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1566-9. doi: 10.1126/science.1189123. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, HDL/*blood ; Diet ; Gene Expression Regulation ; Homeostasis ; Humans ; Introns ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Oligonucleotides, Antisense/pharmacology ; RNA Interference ; Sterol Regulatory Element Binding Protein 1/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Sterol Regulatory Element Binding Proteins/*genetics/metabolism ; Up-Regulation
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    Functional hierarchy and reversibility within the murine spermatogenic stem cell compartment (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-20
    Description: Stem cells support tissue maintenance by balancing self-renewal and differentiation. In mice, it is believed that a homogeneous stem cell population of single spermatogonia supports spermatogenesis, and that differentiation, which is accompanied by the formation of connected cells (cysts) of increasing length, is linear and nonreversible. We evaluated this model with the use of lineage analysis and live imaging, and found that this putative stem cell population is not homogeneous. Instead, the stem cell pool that supports steady-state spermatogenesis is contained within a subpopulation of single spermatogonia. We also found that cysts are not committed to differentiation and appear to recover stem cell potential by fragmentation, and that the fate of individual spermatogonial populations was markedly altered during regeneration after damage. Thus, there are multiple and reversible paths from stem cells to differentiation, and these may also occur in other systems.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981100/" 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/PMC2981100/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, Toshinori -- Sharma, Manju -- Nabeshima, Yo-ichi -- Braun, Robert E -- Yoshida, Shosei -- U54 HD042454/HD/NICHD NIH HHS/ -- U54 HD042454-080002/HD/NICHD NIH HHS/ -- U54 HD4254/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 2;328(5974):62-7. doi: 10.1126/science.1182868. Epub 2010 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Cadherins/genetics/metabolism ; Cell Differentiation ; Cell Lineage ; Gene Expression Profiling ; Glial Cell Line-Derived Neurotrophic Factor Receptors/genetics/metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Nerve Tissue Proteins/genetics/metabolism ; Regeneration ; *Spermatogenesis ; Spermatogonia/*cytology/*physiology ; Stem Cell Niche ; Stem Cells/*cytology/*physiology
    Print ISSN: 0036-8075
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    Calcium-permeable AMPA receptor dynamics mediate fear memory erasure (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-30
    Description: Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001394/" 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/PMC3001394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clem, Roger L -- Huganir, Richard L -- F32 MH087037-01/MH/NIMH NIH HHS/ -- R01 NS036715/NS/NINDS NIH HHS/ -- R01 NS036715-11/NS/NINDS NIH HHS/ -- R01NS036715/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1108-12. doi: 10.1126/science.1195298. Epub 2010 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030604" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Calcium/metabolism ; Conditioning (Psychology) ; *Extinction, Psychological ; Fear/*physiology ; Long-Term Synaptic Depression ; Male ; Memory/*physiology ; Mice ; Mice, Inbred C57BL ; Receptors, AMPA/*metabolism ; Receptors, Glutamate/metabolism ; Thalamus/metabolism
    Print ISSN: 0036-8075
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    Dlg1-PTEN interaction regulates myelin thickness to prevent damaging peripheral nerve overmyelination (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: The thickness of the myelin sheath that insulates axons is fitted for optimal nerve conduction velocity. Here, we show that, in Schwann cells, mammalian disks large homolog 1 (Dlg1) interacts with PTEN (phosphatase and tensin homolog deleted on chromosome 10) to inhibit axonal stimulation of myelination. This mechanism limits myelin sheath thickness and prevents overmyelination in mouse sciatic nerves. Removing this brake results also in myelin outfoldings and demyelination, characteristics of some peripheral neuropathies. Indeed, the Dlg1 brake is no longer functional in a mouse model of Charcot-Marie-Tooth disease. Therefore, negative regulation of myelination appears to be essential for optimization of nerve conduction velocity and myelin maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotter, Laurent -- Ozcelik, Murat -- Jacob, Claire -- Pereira, Jorge A -- Locher, Veronica -- Baumann, Reto -- Relvas, Joao B -- Suter, Ueli -- Tricaud, Nicolas -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1415-8. doi: 10.1126/science.1187735. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell Biology, Department of Biology, Eidgenossische Technische Hochschule (ETH) Zurich, CH-8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448149" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Animals ; Axons/physiology ; Coculture Techniques ; Ganglia, Spinal/cytology ; Membrane Proteins/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Myelin Sheath/*physiology/ultrastructure ; Nerve Tissue Proteins/genetics/*metabolism ; Neural Conduction ; Neuregulin-1/metabolism ; PTEN Phosphohydrolase/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Rats ; Schwann Cells/*physiology ; Sciatic Nerve/physiology
    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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    Bifurcation of Toll-like receptor 9 signaling by adaptor protein 3 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: Endosomal Toll-like receptors (TLRs) 7 and 9 recognize viral pathogens and induce signals leading to the activation of nuclear factor kappaB (NF-kappaB)-dependent proinflammatory cytokines and interferon regulatory factor 7 (IRF7)-dependent type I interferons (IFNs). Recognition of viral nucleic acids by TLR9 requires its cleavage in the endolysosomal compartment. Here, we show that TLR9 signals leading to the activation of type I IFN, but not proinflammatory cytokine genes, require TLR9 trafficking from endosomes to a specialized lysosome-related organelle. Furthermore, we identify adapter protein-3 as the protein complex responsible for the trafficking of TLR9 to this subcellular compartment. Our results reveal an intracellular mechanism for bifurcation of TLR9 signals by selective receptor trafficking within the endosomal system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063333/" 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/PMC3063333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasai, Miwa -- Linehan, Melissa M -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI064705/AI/NIAID NIH HHS/ -- AI081884/AI/NIAID NIH HHS/ -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI054359-07/AI/NIAID NIH HHS/ -- R01 AI064705/AI/NIAID NIH HHS/ -- R01 AI064705-06/AI/NIAID NIH HHS/ -- R01 AI081884/AI/NIAID NIH HHS/ -- R01 AI081884-01A2/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1530-4. doi: 10.1126/science.1187029.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847273" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 3/genetics/*metabolism ; Adaptor Protein Complex beta Subunits ; Animals ; Cells, Cultured ; Cytokines/genetics/immunology/metabolism ; Cytoplasmic Vesicles/metabolism ; Dendritic Cells/*immunology/metabolism ; Endosomes/metabolism ; Interferon Regulatory Factor-7/metabolism ; Interferon Type I/genetics/immunology/metabolism ; Lysosomal-Associated Membrane Protein 2/metabolism ; Macrophages/immunology ; Membrane Transport Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/metabolism ; Oligodeoxyribonucleotides/immunology ; Protein Transport ; Recombinant Fusion Proteins/immunology/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 9/immunology/*metabolism ; Transcriptional Activation ; Vesicle-Associated Membrane Protein 3/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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    Fate mapping analysis reveals that adult microglia derive from primitive macrophages (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719181/" 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/PMC3719181/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ginhoux, Florent -- Greter, Melanie -- Leboeuf, Marylene -- Nandi, Sayan -- See, Peter -- Gokhan, Solen -- Mehler, Mark F -- Conway, Simon J -- Ng, Lai Guan -- Stanley, E Richard -- Samokhvalov, Igor M -- Merad, Miriam -- AI080884/AI/NIAID NIH HHS/ -- CA112100/CA/NCI NIH HHS/ -- CA26504/CA/NCI NIH HHS/ -- CA32551/CA/NCI NIH HHS/ -- HL086899/HL/NHLBI NIH HHS/ -- MH66290/MH/NIMH NIH HHS/ -- NS38902/NS/NINDS NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 CA032551/CA/NCI NIH HHS/ -- R01 HL060714/HL/NHLBI NIH HHS/ -- R01 HL060714-13/HL/NHLBI NIH HHS/ -- R37 CA026504/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):841-5. doi: 10.1126/science.1194637. Epub 2010 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gene and Cell Medicine and the Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA. Florent_ginhoux@immunol.a-star.edu.sg〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/embryology ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Core Binding Factor Alpha 2 Subunit/genetics/metabolism ; Embryo, Mammalian/cytology/physiology ; Female ; Gene Knock-In Techniques ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Homeostasis ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Microglia/*cytology ; Myeloid Progenitor Cells/*cytology ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Yolk Sac/cytology
    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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    Motor control by sensory cortex (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: Classical studies of mammalian movement control define a prominent role for the primary motor cortex. Investigating the mouse whisker system, we found an additional and equally direct pathway for cortical motor control driven by the primary somatosensory cortex. Whereas activity in primary motor cortex directly evokes exploratory whisker protraction, primary somatosensory cortex directly drives whisker retraction, providing a rapid negative feedback signal for sensorimotor integration. Motor control by sensory cortex suggests the need to reevaluate the functional organization of cortical maps.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matyas, Ferenc -- Sreenivasan, Varun -- Marbach, Fred -- Wacongne, Catherine -- Barsy, Boglarka -- Mateo, Celine -- Aronoff, Rachel -- Petersen, Carl C H -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1240-3. doi: 10.1126/science.1195797.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Sensory Processing, Brain Mind Institute, Faculty of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Electric Stimulation ; Feedback, Sensory ; Mice ; Mice, Inbred C57BL ; *Motor Activity ; Motor Cortex/physiology ; Neural Pathways/physiology ; Signal Transduction ; Somatosensory Cortex/*physiology ; Vibrissae/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Altered histone acetylation is associated with age-dependent memory impairment in mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peleg, Shahaf -- Sananbenesi, Farahnaz -- Zovoilis, Athanasios -- Burkhardt, Susanne -- Bahari-Javan, Sanaz -- Agis-Balboa, Roberto Carlos -- Cota, Perla -- Wittnam, Jessica Lee -- Gogol-Doering, Andreas -- Opitz, Lennart -- Salinas-Riester, Gabriella -- Dettenhofer, Markus -- Kang, Hui -- Farinelli, Laurent -- Chen, Wei -- Fischer, Andre -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):753-6. doi: 10.1126/science.1186088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Aging and Cognitive Diseases, European Neuroscience Institute, Grisebach Str. 5, D-37077 Goettingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448184" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Aging/*genetics ; Animals ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; Conditioning (Psychology) ; Epigenesis, Genetic ; Fear ; Gene Expression Profiling ; *Gene Expression Regulation ; Hippocampus/*metabolism ; Histone Deacetylase Inhibitors/metabolism/pharmacology ; Histones/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Lysine/metabolism ; Memory/drug effects ; Memory Disorders/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/genetics/metabolism ; Nuclear Proteins/genetics/metabolism ; Signal Transduction ; Transcription Initiation Site ; Transcription, Genetic ; Up-Regulation
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    A critical role for alpha4betadelta GABAA receptors in shaping learning deficits at puberty in mice (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-20
    Description: The onset of puberty defines a developmental stage when some learning processes are diminished, but the mechanism for this deficit remains unknown. We found that, at puberty, expression of inhibitory alpha4betadelta gamma-aminobutyric acid type A (GABAA) receptors (GABAR) increases perisynaptic to excitatory synapses in CA1 hippocampus. Shunting inhibition via these receptors reduced N-methyl-D-aspartate receptor activation, impairing induction of long-term potentiation (LTP). Pubertal mice also failed to learn a hippocampal, LTP-dependent spatial task that was easily acquired by delta-/- mice. However, the stress steroid THP (3alphaOH-5alpha[beta]-pregnan-20-one), which reduces tonic inhibition at puberty, facilitated learning. Thus, the emergence of alpha4betadelta GABARs at puberty impairs learning, an effect that can be reversed by a stress steroid.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887350/" 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/PMC2887350/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Hui -- Sabaliauskas, Nicole -- Sherpa, Ang -- Fenton, Andre A -- Stelzer, Armin -- Aoki, Chiye -- Smith, Sheryl S -- AA12958/AA/NIAAA NIH HHS/ -- DA09618/DA/NIDA NIH HHS/ -- R01 AA012958/AA/NIAAA NIH HHS/ -- R01 AA012958-08/AA/NIAAA NIH HHS/ -- R01 AA012958-09/AA/NIAAA NIH HHS/ -- R01 DA009618/DA/NIDA NIH HHS/ -- R01 DA009618-13/DA/NIDA NIH HHS/ -- R01 DA009618-14/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1515-8. doi: 10.1126/science.1184245.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, State University of New York (SUNY) Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299596" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/cytology/*metabolism ; Dendrites ; Dendritic Spines/metabolism ; Excitatory Postsynaptic Potentials ; Female ; GABA-A Receptor Antagonists ; *Learning/drug effects ; *Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; N-Methylaspartate/metabolism ; Neural Inhibition ; Patch-Clamp Techniques ; Pregnanolone/pharmacology ; Pyramidal Cells/metabolism ; Receptors, GABA-A/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; *Sexual Maturation ; Spatial Behavior
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    Reversible microbial colonization of germ-free mice reveals the dynamics of IgA immune responses (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-26
    Description: The lower intestine of adult mammals is densely colonized with nonpathogenic (commensal) microbes. Gut bacteria induce protective immune responses, which ensure host-microbial mutualism. The continuous presence of commensal intestinal bacteria has made it difficult to study mucosal immune dynamics. Here, we report a reversible germ-free colonization system in mice that is independent of diet or antibiotic manipulation. A slow (more than 14 days) onset of a long-lived (half-life over 16 weeks), highly specific anticommensal immunoglobulin A (IgA) response in germ-free mice was observed. Ongoing commensal exposure in colonized mice rapidly abrogated this response. Sequential doses lacked a classical prime-boost effect seen in systemic vaccination, but specific IgA induction occurred as a stepwise response to current bacterial exposure, such that the antibody repertoire matched the existing commensal content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923373/" 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/PMC3923373/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hapfelmeier, Siegfried -- Lawson, Melissa A E -- Slack, Emma -- Kirundi, Jorum K -- Stoel, Maaike -- Heikenwalder, Mathias -- Cahenzli, Julia -- Velykoredko, Yuliya -- Balmer, Maria L -- Endt, Kathrin -- Geuking, Markus B -- Curtiss, Roy 3rd -- McCoy, Kathy D -- Macpherson, Andrew J -- R01 AI060557/AI/NIAID NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1705-9. doi: 10.1126/science.1188454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DKF (Maurice Muller Laboratories), MEM, Universitatsklinik fur Viszerale Chirurgie und Medizin (UVCM), University of Bern, 3013 Bern, Switzerland. hapfelmeier@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/biosynthesis/*immunology ; Antibody Specificity ; Colony Count, Microbial ; Dose-Response Relationship, Immunologic ; Escherichia coli/*growth & development/*immunology ; Germ-Free Life ; Half-Life ; Immunoglobulin A/biosynthesis/*immunology ; Immunologic Memory ; Intestinal Mucosa/*immunology/*microbiology ; Intestines/immunology/microbiology ; Mice ; Mice, Inbred C57BL ; Mucous Membrane/immunology ; Plasma Cells/immunology ; Time Factors
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    Transnuclear mice with predefined T cell receptor specificities against Toxoplasma gondii obtained via SCNT (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-10
    Description: Mice that are transgenic for rearranged antigen-specific T cell receptors (TCRs) are essential tools to study T cell development and function. Such TCRs are usually isolated from the relevant T cells after long-term culture, often after repeated antigen stimulation, which unavoidably skews the T cell population used. Random genomic integration of the TCR alpha and beta chain and expression from nonendogenous promoters represent additional drawbacks of transgenics. Using epigenetic reprogramming via somatic cell nuclear transfer, we demonstrated that T cells with predefined specificities against Toxoplasma gondii can be used to generate mouse models that express the TCR from their endogenous loci, without experimentally introduced genetic modification. The relative ease and speed with which such transnuclear models can be obtained holds promise for the construction of other disease models.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940321/" 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/PMC2940321/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirak, Oktay -- Frickel, Eva-Maria -- Grotenbreg, Gijsbert M -- Suh, Heikyung -- Jaenisch, Rudolf -- Ploegh, Hidde L -- R01 GM062502/GM/NIGMS NIH HHS/ -- R01 GM062502-08/GM/NIGMS NIH HHS/ -- R01-HD045022/HD/NICHD NIH HHS/ -- R37 AI033456/AI/NIAID NIH HHS/ -- R37 AI033456-17/AI/NIAID NIH HHS/ -- R37-CA084198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):243-8. doi: 10.1126/science.1178590.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. kirak@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Protozoan/*immunology ; CD8-Positive T-Lymphocytes/immunology ; Embryonic Stem Cells ; Epitopes, T-Lymphocyte ; Female ; Genes, T-Cell Receptor alpha ; Genes, T-Cell Receptor beta ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; *Mice, Transgenic ; Molecular Sequence Data ; *Nuclear Transfer Techniques ; Protozoan Proteins/genetics/immunology ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*immunology ; Toxoplasma/*immunology ; Toxoplasmosis, Animal/*immunology
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    Exploitation of the intestinal microflora by the parasitic nematode Trichuris muris (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-12
    Description: The inhabitants of the mammalian gut are not always relatively benign commensal bacteria but may also include larger and more parasitic organisms, such as worms and protozoa. At some level, all these organisms are capable of interacting with each other. We found that successful establishment of the chronically infecting parasitic nematode Trichuris muris in the large intestine of mice is dependent on microflora and coincident with modulation of the host immune response. By reducing the number of bacteria in the host animal, we significantly reduced the number of hatched T. muris eggs. Critical interactions between bacteria (microflora) and parasites (macrofauna) introduced a new dynamic to the intestinal niche, which has fundamental implications for our current concepts of intestinal homeostasis and regulation of immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428897/" 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/PMC3428897/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayes, K S -- Bancroft, A J -- Goldrick, M -- Portsmouth, C -- Roberts, I S -- Grencis, R K -- 083620/Wellcome Trust/United Kingdom -- 083620Z/Wellcome Trust/United Kingdom -- G0601205/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1391-4. doi: 10.1126/science.1187703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538949" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Adhesins, Escherichia coli/metabolism ; Animals ; Anti-Bacterial Agents/pharmacology ; Antibodies, Helminth/biosynthesis ; *Bacterial Physiological Phenomena ; Cecum/microbiology/parasitology ; Cytokines/metabolism ; Escherichia coli/physiology ; Fimbriae Proteins/metabolism ; Fimbriae, Bacterial/physiology ; Fluoroquinolones/pharmacology ; Host-Parasite Interactions ; Intestine, Large/*microbiology/*parasitology ; Mice ; Mice, Inbred AKR ; Mice, Inbred C57BL ; Mice, SCID ; Ovum/physiology ; Th2 Cells/immunology ; Trichuriasis/immunology/microbiology/*parasitology ; Trichuris/embryology/*physiology
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    The junctional adhesion molecule JAML is a costimulatory receptor for epithelial gammadelta T cell activation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Gammadelta T cells present in epithelial tissues provide a crucial first line of defense against environmental insults, including infection, trauma, and malignancy, yet the molecular events surrounding their activation remain poorly defined. Here we identify an epithelial gammadelta T cell-specific costimulatory molecule, junctional adhesion molecule-like protein (JAML). Binding of JAML to its ligand Coxsackie and adenovirus receptor (CAR) provides costimulation leading to cellular proliferation and cytokine and growth factor production. Inhibition of JAML costimulation leads to diminished gammadelta T cell activation and delayed wound closure akin to that seen in the absence of gammadelta T cells. Our results identify JAML as a crucial component of epithelial gammadelta T cell biology and have broader implications for CAR and JAML in tissue homeostasis and repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943937/" 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/PMC2943937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witherden, Deborah A -- Verdino, Petra -- Rieder, Stephanie E -- Garijo, Olivia -- Mills, Robyn E -- Teyton, Luc -- Fischer, Wolfgang H -- Wilson, Ian A -- Havran, Wendy L -- AI064811/AI/NIAID NIH HHS/ -- AI42266/AI/NIAID NIH HHS/ -- AI52257/AI/NIAID NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- NS057096/NS/NINDS NIH HHS/ -- R01 AI036964/AI/NIAID NIH HHS/ -- R01 AI052257/AI/NIAID NIH HHS/ -- R01 AI052257-05/AI/NIAID NIH HHS/ -- R01 AI064811/AI/NIAID NIH HHS/ -- R01 AI064811-05/AI/NIAID NIH HHS/ -- R01 GM080301/GM/NIGMS NIH HHS/ -- R37 AI042266/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1205-10. doi: 10.1126/science.1192698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813954" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cell Adhesion Molecules/*metabolism ; Cell Line ; Cell Proliferation ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Cytokines/metabolism ; Epidermis/cytology/*immunology/injuries ; Epithelial Cells ; Epithelium/immunology/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/metabolism ; Ligands ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Binding ; Receptors, Antigen, T-Cell, gamma-delta/*immunology/metabolism ; Receptors, Virus/*metabolism ; T-Lymphocyte Subsets/*immunology/*metabolism ; Wound Healing
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    PiggyBac transposon mutagenesis: a tool for cancer gene discovery in mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Transposons are mobile DNA segments that can disrupt gene function by inserting in or near genes. Here, we show that insertional mutagenesis by the PiggyBac transposon can be used for cancer gene discovery in mice. PiggyBac transposition in genetically engineered transposon-transposase mice induced cancers whose type (hematopoietic versus solid) and latency were dependent on the regulatory elements introduced into transposons. Analysis of 63 hematopoietic tumors revealed that PiggyBac is capable of genome-wide mutagenesis. The PiggyBac screen uncovered many cancer genes not identified in previous retroviral or Sleeping Beauty transposon screens, including Spic, which encodes a PU.1-related transcription factor, and Hdac7, a histone deacetylase gene. PiggyBac and Sleeping Beauty have different integration preferences. To maximize the utility of the tool, we engineered 21 mouse lines to be compatible with both transposon systems in constitutive, tissue- or temporal-specific mutagenesis. Mice with different transposon types, copy numbers, and chromosomal locations support wide applicability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719098/" 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/PMC3719098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rad, Roland -- Rad, Lena -- Wang, Wei -- Cadinanos, Juan -- Vassiliou, George -- Rice, Stephen -- Campos, Lia S -- Yusa, Kosuke -- Banerjee, Ruby -- Li, Meng Amy -- de la Rosa, Jorge -- Strong, Alexander -- Lu, Dong -- Ellis, Peter -- Conte, Nathalie -- Yang, Fang Tang -- Liu, Pentao -- Bradley, Allan -- 077186/Wellcome Trust/United Kingdom -- 079643/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1104-7. doi: 10.1126/science.1193004. Epub 2010 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Genome Campus, Hinxton-Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Transposable Elements ; *Genes, Neoplasm ; Genetic Testing/*methods ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Mutagenesis, Insertional ; Neoplasms/genetics ; Oncogenes ; Promoter Regions, Genetic
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    An essential developmental checkpoint for production of the T cell lineage (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: In early T cell development, progenitors retaining the potential to generate myeloid and natural killer lineages are eventually determined to a specific T cell lineage. The molecular mechanisms that drive this determination step remain unclarified. We show that, when murine hematopoietic progenitors were cultured on immobilized Notch ligand DLL4 protein in the presence of a cocktail of cytokines including interleukin-7, progenitors developing toward T cells were arrested and the arrested cells entered a self-renewal cycle, maintaining non-T lineage potentials. Reduced concentrations of interleukin-7 promoted T cell lineage determination. A similar arrest and self-renewal of progenitors were observed in thymocytes of mice deficient in the transcription factor Bcl11b. Our study thus identifies the earliest checkpoint during T cell development and shows that it is Bcl11b-dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikawa, Tomokatsu -- Hirose, Satoshi -- Masuda, Kyoko -- Kakugawa, Kiyokazu -- Satoh, Rumi -- Shibano-Satoh, Asako -- Kominami, Ryo -- Katsura, Yoshimoto -- Kawamoto, Hiroshi -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):93-6. doi: 10.1126/science.1188995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Lymphocyte Development, RIKEN Research Center for Allergy and Immunology, Yokohama 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Gene Expression Regulation, Developmental ; Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Hematopoietic Stem Cells/cytology/*physiology ; Interleukin-7/metabolism ; Liver/embryology ; *Lymphopoiesis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Precursor Cells, T-Lymphoid/cytology/*physiology ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/*cytology/*physiology ; Tumor Suppressor Proteins/genetics/*metabolism ; Up-Regulation
    Print ISSN: 0036-8075
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    MiR-33 contributes to the regulation of cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114628/" 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/PMC3114628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rayner, Katey J -- Suarez, Yajaira -- Davalos, Alberto -- Parathath, Saj -- Fitzgerald, Michael L -- Tamehiro, Norimasa -- Fisher, Edward A -- Moore, Kathryn J -- Fernandez-Hernando, Carlos -- 1P30HL101270-01/HL/NHLBI NIH HHS/ -- P30 HL101270/HL/NHLBI NIH HHS/ -- R01 AG020255/AG/NIA NIH HHS/ -- R01 AG020255-09/AG/NIA NIH HHS/ -- R01AG02055/AG/NIA NIH HHS/ -- R01HL074136/HL/NHLBI NIH HHS/ -- R01HL084312/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1570-3. doi: 10.1126/science.1189862. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466885" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/metabolism ; Animals ; Apolipoprotein A-I/metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Hypercholesterolemia/genetics/metabolism ; Introns ; Lipoproteins/genetics/metabolism ; Lipoproteins, HDL/blood/*metabolism ; Liver/*metabolism ; Macrophages/metabolism ; Macrophages, Peritoneal/metabolism ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Proteins/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Transfection
    Print ISSN: 0036-8075
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    ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-22
    Description: Elevated leukocyte cell numbers (leukocytosis), and monocytes in particular, promote atherosclerosis; however, how they become increased is poorly understood. Mice deficient in the adenosine triphosphate-binding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow. Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis. The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoietic stem and multipotential progenitor cells and connect expansion of these populations with leukocytosis and accelerated atherosclerosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032591/" 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/PMC3032591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yvan-Charvet, Laurent -- Pagler, Tamara -- Gautier, Emmanuel L -- Avagyan, Serine -- Siry, Read L -- Han, Seongah -- Welch, Carrie L -- Wang, Nan -- Randolph, Gwendalyn J -- Snoeck, Hans W -- Tall, Alan R -- HL54591/HL/NHLBI NIH HHS/ -- R01 AG029626/AG/NIA NIH HHS/ -- R01 AI049653/AI/NIAID NIH HHS/ -- R01 AI049653-09/AI/NIAID NIH HHS/ -- R01 AI049653-10/AI/NIAID NIH HHS/ -- R01 AI061741/AI/NIAID NIH HHS/ -- R01 AI061741-03/AI/NIAID NIH HHS/ -- R01 AI061741-04/AI/NIAID NIH HHS/ -- R01A1061741/PHS HHS/ -- R01AG016327/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1689-93. doi: 10.1126/science.1189731. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA. ly2159@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488992" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Apolipoprotein A-I/genetics/metabolism ; Atherosclerosis/metabolism/*physiopathology/therapy ; Bone Marrow Transplantation ; Cell Proliferation ; Cells, Cultured ; Cholesterol/*metabolism ; Hematopoietic Stem Cells/*physiology ; Hypercholesterolemia/metabolism ; Leukocytosis/metabolism/*physiopathology/therapy ; Lipoproteins/genetics/*metabolism ; Lipoproteins, HDL/*metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Multipotent Stem Cells/physiology ; Myeloid Progenitor Cells/*physiology ; Myeloproliferative Disorders/metabolism/physiopathology/therapy ; Phenotype ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Receptors, Interleukin-3/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Neural crest-derived pericytes promote egress of mature thymocytes at the corticomedullary junction (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-24
    Description: T cell egress from the thymus is essential for adaptive immunity, yet the requirements for and sites of egress are incompletely understood. We have shown that transgenic expression of sphingosine-1-phosphate receptor-1 (S1P1) in immature thymocytes leads to their perivascular accumulation and premature release into circulation. Using an intravascular procedure to label emigrating cells, we found that mature thymocytes exit via blood vessels at the corticomedullary junction. By deleting sphingosine kinases in neural crest-derived pericytes, we provide evidence that these specialized vessel-ensheathing cells contribute to the S1P that promotes thymic egress. Lymphatic endothelial cell-derived S1P was not required. These studies identify the major thymic egress route and suggest a role for pericytes in promoting reverse transmigration of cells across blood vessel endothelium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3107339/" 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/PMC3107339/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zachariah, Marcus A -- Cyster, Jason G -- AI74847/AI/NIAID NIH HHS/ -- R01 AI074847/AI/NIAID NIH HHS/ -- R01 AI074847-02/AI/NIAID NIH HHS/ -- R01 AI074847-03/AI/NIAID NIH HHS/ -- R01 AI074847-04/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1129-35. doi: 10.1126/science.1188222. Epub 2010 Apr 22.〈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, HSE1001, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Blood Vessels/cytology/*physiology ; Cell Movement ; Endothelial Cells/physiology ; Endothelium, Vascular/cytology/physiology ; Flow Cytometry ; Fluorescent Antibody Technique ; Kruppel-Like Transcription Factors/genetics/physiology ; Lymphatic Vessels/cytology/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neural Crest/cytology ; Pericytes/metabolism/*physiology ; Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism ; Receptors, Lysosphingolipid/genetics/*physiology ; T-Lymphocytes/cytology/metabolism/*physiology ; T-Lymphocytes, Regulatory/immunology/physiology ; Thymus Gland/*blood supply/*cytology
    Print ISSN: 0036-8075
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    Protein kinase C-theta mediates negative feedback on regulatory T cell function (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: T cell receptor (TCR)-dependent regulatory T cell (Treg) activity controls effector T cell (Teff) function and is inhibited by the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Protein kinase C-theta (PKC-theta) recruitment to the immunological synapse is required for full Teff activation. In contrast, PKC-theta was sequestered away from the Treg immunological synapse. Furthermore, PKC-theta blockade enhanced Treg function, demonstrating PKC-theta inhibits Treg-mediated suppression. Inhibition of PKC-theta protected Treg from inactivation by TNF-alpha, restored activity of defective Treg from rheumatoid arthritis patients, and enhanced protection of mice from inflammatory colitis. Treg freed of PKC-theta-mediated inhibition can function in the presence of inflammatory cytokines and thus have therapeutic potential in control of inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905626/" 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/PMC2905626/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zanin-Zhorov, Alexandra -- Ding, Yi -- Kumari, Sudha -- Attur, Mukundan -- Hippen, Keli L -- Brown, Maryanne -- Blazar, Bruce R -- Abramson, Steven B -- Lafaille, Juan J -- Dustin, Michael L -- P01 AI056299/AI/NIAID NIH HHS/ -- PN2 EY016586/EY/NEI NIH HHS/ -- PN2 EY016586-06/EY/NEI NIH HHS/ -- R01 AI055037/AI/NIAID NIH HHS/ -- R01 AI055037-06A1/AI/NIAID NIH HHS/ -- R01 AI43542/AI/NIAID NIH HHS/ -- R01 HL056067/HL/NHLBI NIH HHS/ -- R37 AI043542/AI/NIAID NIH HHS/ -- R37 AI043542-12/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):372-6. doi: 10.1126/science.1186068. Epub 2010 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Helen and Martin Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, Department of Pathology, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339032" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Arthritis, Rheumatoid/immunology ; Colitis/immunology/prevention & control ; Enzyme Inhibitors/pharmacology ; Feedback, Physiological ; Humans ; Immunological Synapses/*immunology ; Inflammation/*immunology ; Interferon-gamma/metabolism ; Isoenzymes/antagonists & inhibitors/*metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Protein Kinase C/antagonists & inhibitors/*metabolism ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/*immunology/metabolism ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Young Adult
    Print ISSN: 0036-8075
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    Human-restricted bacterial pathogens block shedding of epithelial cells by stimulating integrin activation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Colonization of mucosal surfaces is the key initial step in most bacterial infections. One mechanism protecting the mucosa is the rapid shedding of epithelial cells, also termed exfoliation, but it is unclear how pathogens counteract this process. We found that carcinoembryonic antigen (CEA)-binding bacteria colonized the urogenital tract of CEA transgenic mice, but not of wild-type mice, by suppressing exfoliation of mucosal cells. CEA binding triggered de novo expression of the transforming growth factor receptor CD105, changing focal adhesion composition and activating beta1 integrins. This manipulation of integrin inside-out signaling promotes efficient mucosal colonization and represents a potential target to prevent or cure bacterial infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muenzner, Petra -- Bachmann, Verena -- Zimmermann, Wolfgang -- Hentschel, Jochen -- Hauck, Christof R -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1197-201. doi: 10.1126/science.1190892.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lehrstuhl Zellbiologie, Fachbereich Biologie, Universitat Konstanz, 78457 Konstanz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/metabolism ; Antigens, CD/metabolism ; Carcinoembryonic Antigen/genetics/*metabolism ; Cytoskeletal Proteins/metabolism ; Epithelial Cells/microbiology/*pathology ; Female ; Focal Adhesions ; GPI-Linked Proteins ; Glycoproteins/metabolism ; Gonorrhea/*microbiology ; Humans ; Integrin beta Chains/*metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mucous Membrane/microbiology ; Neisseria gonorrhoeae/isolation & purification/*metabolism/*pathogenicity ; Receptors, Cell Surface/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Vagina/cytology/*microbiology/pathology ; Zyxin
    Print ISSN: 0036-8075
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