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  • Mice  (1,295)
  • American Association for the Advancement of Science (AAAS)  (1,295)
  • Annual Reviews
  • Oxford University Press
  • 2010-2014  (826)
  • 1980-1984  (469)
  • 1955-1959
  • 1930-1934
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  • 1
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    Nebulin and N-WASP cooperate to cause IGF-1-induced sarcomeric actin filament formation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-15
    Description: Insulin-like growth factor 1 (IGF-1) induces skeletal muscle maturation and enlargement (hypertrophy). These responses require protein synthesis and myofibril formation (myofibrillogenesis). However, the signaling mechanisms of myofibrillogenesis remain obscure. We found that IGF-1-induced phosphatidylinositol 3-kinase-Akt signaling formed a complex of nebulin and N-WASP at the Z bands of myofibrils by interfering with glycogen synthase kinase-3beta in mice. Although N-WASP is known to be an activator of the Arp2/3 complex to form branched actin filaments, the nebulin-N-WASP complex caused actin nucleation for unbranched actin filament formation from the Z bands without the Arp2/3 complex. Furthermore, N-WASP was required for IGF-1-induced muscle hypertrophy. These findings present the mechanisms of IGF-1-induced actin filament formation in myofibrillogenesis required for muscle maturation and hypertrophy and a mechanism of actin nucleation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takano, Kazunori -- Watanabe-Takano, Haruko -- Suetsugu, Shiro -- Kurita, Souichi -- Tsujita, Kazuya -- Kimura, Sumiko -- Karatsu, Takashi -- Takenawa, Tadaomi -- Endo, Takeshi -- New York, N.Y. -- Science. 2010 Dec 10;330(6010):1536-40. doi: 10.1126/science.1197767.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Graduate School of Science, Chiba University, 1-33 Yayoicho, Inageku, Chiba 263-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21148390" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actins/*metabolism ; Animals ; COS Cells ; Cercopithecus aethiops ; Hypertrophy ; Insulin-Like Growth Factor I/*metabolism ; Mice ; Mice, Inbred ICR ; *Muscle Development ; Muscle Proteins/chemistry/*metabolism ; Muscle, Skeletal/metabolism/pathology ; Myofibrils/metabolism ; Phosphatidylinositol 3-Kinase/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Sarcomeres/*metabolism ; Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal/chemistry/*metabolism ; src Homology Domains
    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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    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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  • 3
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    Beta2-adrenergic receptor redistribution in heart failure changes cAMP compartmentation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: The beta1- and beta2-adrenergic receptors (betaARs) on the surface of cardiomyocytes mediate distinct effects on cardiac function and the development of heart failure by regulating production of the second messenger cyclic adenosine monophosphate (cAMP). The spatial localization in cardiomyocytes of these betaARs, which are coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins), and the functional implications of their localization have been unclear. We combined nanoscale live-cell scanning ion conductance and fluorescence resonance energy transfer microscopy techniques and found that, in cardiomyocytes from healthy adult rats and mice, spatially confined beta2AR-induced cAMP signals are localized exclusively to the deep transverse tubules, whereas functional beta1ARs are distributed across the entire cell surface. In cardiomyocytes derived from a rat model of chronic heart failure, beta2ARs were redistributed from the transverse tubules to the cell crest, which led to diffuse receptor-mediated cAMP signaling. Thus, the redistribution of beta(2)ARs in heart failure changes compartmentation of cAMP and might contribute to the failing myocardial phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nikolaev, Viacheslav O -- Moshkov, Alexey -- Lyon, Alexander R -- Miragoli, Michele -- Novak, Pavel -- Paur, Helen -- Lohse, Martin J -- Korchev, Yuri E -- Harding, Sian E -- Gorelik, Julia -- 084064/Wellcome Trust/United Kingdom -- BB/D020875/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500373/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1653-7. doi: 10.1126/science.1185988. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism/ultrastructure ; Chronic Disease ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytosol/metabolism ; Fluorescence Resonance Energy Transfer ; Heart Failure/*metabolism/*pathology ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Microscopy/methods ; Myocytes, Cardiac/*metabolism/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-1/genetics/metabolism ; Receptors, Adrenergic, beta-2/genetics/*metabolism ; Sarcolemma/*metabolism/ultrastructure ; Signal Transduction
    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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    Immunology. Mouse studies challenge rare immune cell's powers (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1595. doi: 10.1126/science.329.5999.1595.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929824" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Antibodies/immunology ; *Antigen Presentation ; Antigen-Presenting Cells/immunology ; Basophils/*immunology ; Dendritic Cells/immunology ; Helminths/immunology ; Lymph Nodes/immunology ; Mice ; Th2 Cells/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Differential arginylation of actin isoforms is regulated by coding sequence-dependent degradation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: The mammalian cytoskeletal proteins beta- and gamma-actin are highly homologous, but only beta-actin is amino-terminally arginylated in vivo, which regulates its function. We examined the metabolic fate of exogenously expressed arginylated and nonarginylated actin isoforms. Arginylated gamma-actin, unlike beta-, was highly unstable and was selectively ubiquitinated and degraded in vivo. This instability was regulated by the differences in the nucleotide coding sequence between the two actin isoforms, which conferred different translation rates. gamma-actin was translated more slowly than beta-actin, and this slower processing resulted in the exposure of a normally hidden lysine residue for ubiquitination, leading to the preferential degradation of gamma-actin upon arginylation. This degradation mechanism, coupled to nucleotide coding sequence, may regulate protein arginylation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941909/" 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/PMC2941909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Fangliang -- Saha, Sougata -- Shabalina, Svetlana A -- Kashina, Anna -- 5R01HL084419/HL/NHLBI NIH HHS/ -- R01 HL084419/HL/NHLBI NIH HHS/ -- R01 HL084419-03/HL/NHLBI NIH HHS/ -- R01 HL084419-03S1/HL/NHLBI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1534-7. doi: 10.1126/science.1191701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847274" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/genetics/*metabolism ; Amino Acid Sequence ; Animals ; Arginine/*metabolism ; Cell Line ; Cell Line, Tumor ; *Codon ; Humans ; Lysine/metabolism ; Mice ; Nucleic Acid Conformation ; Proteasome Endopeptidase Complex/metabolism ; Protein Biosynthesis ; Protein Folding ; Protein Isoforms/chemistry/genetics/metabolism ; *Protein Modification, Translational ; Protein Stability ; RNA, Messenger/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Ubiquitination
    Print ISSN: 0036-8075
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  • 6
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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
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  • 7
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    Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: Gain-of-function mutations in Kir6.2 (KCNJ11), the pore-forming subunit of the adenosine triphosphate (ATP)-sensitive potassium (KATP) channel, cause neonatal diabetes. Many patients also suffer from hypotonia (weak and flaccid muscles) and balance problems. The diabetes arises from suppressed insulin secretion by overactive KATP channels in pancreatic beta-cells, but the source of the motor phenotype is unknown. By using mice carrying a human Kir6.2 mutation (Val59--〉Met59) targeted to either muscle or nerve, we show that analogous motor impairments originate in the central nervous system rather than in muscle or peripheral nerves. We also identify locomotor hyperactivity as a feature of KATP channel overactivity. These findings suggest that drugs targeted against neuronal, rather than muscle, KATP channels are needed to treat the motor deficits and that such drugs require high blood-brain barrier permeability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Rebecca H -- McTaggart, James S -- Webster, Richard -- Mannikko, Roope -- Iberl, Michaela -- Sim, Xiu Li -- Rorsman, Patrik -- Glitsch, Maike -- Beeson, David -- Ashcroft, Frances M -- 084655/Wellcome Trust/United Kingdom -- G0701521/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):458-61. doi: 10.1126/science.1186146. Epub 2010 Jul 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595581" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Ataxia/physiopathology ; Diabetes Mellitus/*genetics/metabolism/physiopathology ; Female ; Gene Targeting ; Humans ; Infant, Newborn ; Male ; Membrane Potentials ; Mice ; Mice, Transgenic ; Motor Activity ; Muscle Hypotonia/*genetics/metabolism/physiopathology ; Muscle Strength ; Muscles/*metabolism ; Neurons/*metabolism ; Patch-Clamp Techniques ; Postural Balance ; Potassium Channels, Inwardly Rectifying/*genetics/*metabolism ; Purkinje Cells/physiology ; Receptors, Drug/metabolism ; Sulfonylurea Receptors ; Syndrome
    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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  • 8
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    Extending healthy life span--from yeast to humans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-17
    Description: When the food intake of organisms such as yeast and rodents is reduced (dietary restriction), they live longer than organisms fed a normal diet. A similar effect is seen when the activity of nutrient-sensing pathways is reduced by mutations or chemical inhibitors. In rodents, both dietary restriction and decreased nutrient-sensing pathway activity can lower the incidence of age-related loss of function and disease, including tumors and neurodegeneration. Dietary restriction also increases life span and protects against diabetes, cancer, and cardiovascular disease in rhesus monkeys, and in humans it causes changes that protect against these age-related pathologies. Tumors and diabetes are also uncommon in humans with mutations in the growth hormone receptor, and natural genetic variants in nutrient-sensing pathways are associated with increased human life span. Dietary restriction and reduced activity of nutrient-sensing pathways may thus slow aging by similar mechanisms, which have been conserved during evolution. We discuss these findings and their potential application to prevention of age-related disease and promotion of healthy aging in humans, and the challenge of possible negative side effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607354/" 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/PMC3607354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontana, Luigi -- Partridge, Linda -- Longo, Valter D -- AG025135/AG/NIA NIH HHS/ -- AG20642/AG/NIA NIH HHS/ -- GM075308/GM/NIGMS NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30DK056341/DK/NIDDK NIH HHS/ -- R01 AG020642/AG/NIA NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):321-6. doi: 10.1126/science.1172539.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Geriatrics and Nutritional Science, Washington University School of Medicine, St. Louis, MO 63110, USA. lfontana@dom.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20395504" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Caenorhabditis elegans/genetics/physiology ; *Caloric Restriction ; Drosophila/genetics/physiology ; Eating ; Haplorhini ; Humans ; *Longevity ; Mice ; Saccharomyces cerevisiae/genetics/physiology ; *Signal Transduction
    Print ISSN: 0036-8075
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  • 9
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    Tuberculosis: what we don't know can, and does, hurt us (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Mycobacterium tuberculosis has a penetrance of its host population that would be the envy of most human pathogens. About one-third of the human population would have a positive skin test for the infection and is thus thought to harbor the bacterium. Globally, 22 "high-burden" countries account for more than 80% of the active tuberculosis cases in the world, which shows the inequitable distribution of the disease. There is no effective vaccine against infection, and current drug therapies are fraught with problems, predominantly because of the protracted nature of the treatment and the increasing occurrence of drug resistance. Here we focus on the biology of the host-pathogen interaction and discuss new and evolving strategies for intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872107/" 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/PMC2872107/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, David G -- Barry, Clifton E 3rd -- Flynn, JoAnne L -- AI057086/AI/NIAID NIH HHS/ -- AI067027/AI/NIAID NIH HHS/ -- AI080651/AI/NIAID NIH HHS/ -- AI50732/AI/NIAID NIH HHS/ -- HL055936/HL/NHLBI NIH HHS/ -- HL075845/HL/NHLBI NIH HHS/ -- HL092883/HL/NHLBI NIH HHS/ -- HL100928/HL/NHLBI NIH HHS/ -- HL71241/HL/NHLBI NIH HHS/ -- R01 AI037859/AI/NIAID NIH HHS/ -- R01 AI050732/AI/NIAID NIH HHS/ -- R01 AI050732-07/AI/NIAID NIH HHS/ -- R01 AI057086/AI/NIAID NIH HHS/ -- R01 AI057086-06A2/AI/NIAID NIH HHS/ -- R01 AI067027/AI/NIAID NIH HHS/ -- R01 AI067027-05/AI/NIAID NIH HHS/ -- R01 AI080651/AI/NIAID NIH HHS/ -- R01 AI080651-02/AI/NIAID NIH HHS/ -- R01 HL055936/HL/NHLBI NIH HHS/ -- R01 HL055936-14/HL/NHLBI NIH HHS/ -- R01 HL075845/HL/NHLBI NIH HHS/ -- R01 HL075845-05/HL/NHLBI NIH HHS/ -- R01 HL100928/HL/NHLBI NIH HHS/ -- R01 HL100928-01/HL/NHLBI NIH HHS/ -- R33 HL092883/HL/NHLBI NIH HHS/ -- R33 HL092883-02/HL/NHLBI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 May 14;328(5980):852-6. doi: 10.1126/science.1184784.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. dgr8@cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antitubercular Agents/pharmacology/therapeutic use ; *BCG Vaccine/administration & dosage/immunology ; Biomarkers ; Disease Models, Animal ; Drug Discovery ; Drug Therapy, Combination ; Host-Pathogen Interactions ; Humans ; Mice ; *Mycobacterium tuberculosis/growth & development/immunology/metabolism ; Public Health Practice ; *Tuberculosis/drug therapy/immunology/microbiology/prevention & control ; Vaccination
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  • 10
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    Covering a broad dynamic range: information processing at the erythropoietin receptor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-22
    Description: Cell surface receptors convert extracellular cues into receptor activation, thereby triggering intracellular signaling networks and controlling cellular decisions. A major unresolved issue is the identification of receptor properties that critically determine processing of ligand-encoded information. We show by mathematical modeling of quantitative data and experimental validation that rapid ligand depletion and replenishment of the cell surface receptor are characteristic features of the erythropoietin (Epo) receptor (EpoR). The amount of Epo-EpoR complexes and EpoR activation integrated over time corresponds linearly to ligand input; this process is carried out over a broad range of ligand concentrations. This relation depends solely on EpoR turnover independent of ligand binding, which suggests an essential role of large intracellular receptor pools. These receptor properties enable the system to cope with basal and acute demand in the hematopoietic system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becker, Verena -- Schilling, Marcel -- Bachmann, Julie -- Baumann, Ute -- Raue, Andreas -- Maiwald, Thomas -- Timmer, Jens -- Klingmuller, Ursula -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1404-8. doi: 10.1126/science.1184913. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division Systems Biology of Signal Transduction, DKFZ-ZMBH Alliance, German Cancer Research Center, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488988" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*metabolism ; Computer Simulation ; Endocytosis ; Epoetin Alfa ; Erythropoietin/metabolism/pharmacology ; Kinetics ; Ligands ; Mice ; Models, Biological ; Protein Binding ; Receptors, Erythropoietin/*metabolism ; Recombinant Proteins ; Signal Transduction
    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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  • 11
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    Identification of RACK1 and protein kinase Calpha as integral components of the mammalian circadian clock (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: At the core of the mammalian circadian clock is a negative feedback loop in which the dimeric transcription factor CLOCK-BMAL1 drives processes that in turn suppress its transcriptional activity. To gain insight into the mechanisms of circadian feedback, we analyzed mouse protein complexes containing BMAL1. Receptor for activated C kinase-1 (RACK1) and protein kinase C-alpha (PKCalpha) were recruited in a circadian manner into a nuclear BMAL1 complex during the negative feedback phase of the cycle. Overexpression of RACK1 and PKCalpha suppressed CLOCK-BMAL1 transcriptional activity, and RACK1 stimulated phosphorylation of BMAL1 by PKCalpha in vitro. Depletion of endogenous RACK1 or PKCalpha from fibroblasts shortened the circadian period, demonstrating that both molecules function in the clock oscillatory mechanism. Thus, the classical PKC signaling pathway is not limited to relaying external stimuli but is rhythmically activated by internal processes, forming an integral part of the circadian feedback loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robles, Maria S -- Boyault, Cyril -- Knutti, Darko -- Padmanabhan, Kiran -- Weitz, Charles J -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):463-6. doi: 10.1126/science.1180067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093473" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Feedback, Physiological ; Fibroblasts/metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Neuropeptides/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinase C-alpha/*metabolism ; RNA Interference ; Signal Transduction ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Video-rate molecular imaging in vivo with stimulated Raman scattering (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Optical imaging in vivo with molecular specificity is important in biomedicine because of its high spatial resolution and sensitivity compared with magnetic resonance imaging. Stimulated Raman scattering (SRS) microscopy allows highly sensitive optical imaging based on vibrational spectroscopy without adding toxic or perturbative labels. However, SRS imaging in living animals and humans has not been feasible because light cannot be collected through thick tissues, and motion-blur arises from slow imaging based on backscattered light. In this work, we enable in vivo SRS imaging by substantially enhancing the collection of the backscattered signal and increasing the imaging speed by three orders of magnitude to video rate. This approach allows label-free in vivo imaging of water, lipid, and protein in skin and mapping of penetration pathways of topically applied drugs in mice and humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462359/" 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/PMC3462359/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saar, Brian G -- Freudiger, Christian W -- Reichman, Jay -- Stanley, C Michael -- Holtom, Gary R -- Xie, X Sunney -- 1R01EB010244-01/EB/NIBIB NIH HHS/ -- R01 EB010244/EB/NIBIB NIH HHS/ -- R01 EB010244-02/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1368-70. doi: 10.1126/science.1197236.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127249" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Cutaneous ; Animals ; Capillaries ; Dimethyl Sulfoxide/administration & dosage/pharmacokinetics ; Epidermis/chemistry/metabolism ; Erythrocytes/physiology ; Humans ; Imaging, Three-Dimensional ; Light ; Lipids ; Male ; Mice ; Mice, Nude ; Molecular Imaging/*methods ; Skin/blood supply/*chemistry/*metabolism ; Spectrum Analysis, Raman/*methods ; Time Factors ; Vitamin A/administration & dosage/pharmacokinetics ; Water
    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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    Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-26
    Description: Ghrelin is a gastric peptide hormone that stimulates weight gain in vertebrates. The biological activities of ghrelin require octanoylation of the peptide on Ser(3), an unusual posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). Here, we describe the design, synthesis, and characterization of GO-CoA-Tat, a peptide-based bisubstrate analog that antagonizes GOAT. GO-CoA-Tat potently inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-CoA-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin-deficient mice, supporting the concept that its beneficial metabolic effects are due specifically to GOAT inhibition. In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, Brad P -- Hwang, Yousang -- Taylor, Martin S -- Kirchner, Henriette -- Pfluger, Paul T -- Bernard, Vincent -- Lin, Yu-yi -- Bowers, Erin M -- Mukherjee, Chandrani -- Song, Woo-Jin -- Longo, Patti A -- Leahy, Daniel J -- Hussain, Mehboob A -- Tschop, Matthias H -- Boeke, Jef D -- Cole, Philip A -- P01 CA016519/CA/NCI NIH HHS/ -- P01 CA016519-35/CA/NCI NIH HHS/ -- P30 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637-05/DK/NIDDK NIH HHS/ -- R01 DK081472/DK/NIDDK NIH HHS/ -- R01 DK081472-01A1/DK/NIDDK NIH HHS/ -- R01 DK081472-02/DK/NIDDK NIH HHS/ -- R01 DK081472-03/DK/NIDDK NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-04/GM/NIGMS NIH HHS/ -- R01 GM062437-11/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1689-92. doi: 10.1126/science.1196154. Epub 2010 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21097901" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Acyltransferases/*antagonists & inhibitors ; Animals ; Cell Survival/drug effects ; Drug Design ; Enzyme Inhibitors/chemical synthesis/*pharmacology/toxicity ; Ghrelin/deficiency/genetics/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; HeLa Cells ; Homeostasis ; Humans ; Insulin/metabolism ; Ion Channels/metabolism ; Islets of Langerhans/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Peptides/chemical synthesis/*pharmacology/toxicity ; Weight Gain/*drug effects
    Print ISSN: 0036-8075
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  • 14
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    Developmental biology. Branching takes nerve (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, Jason R -- Hogan, Brigid L M -- R37 HL071303/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1610-1. doi: 10.1126/science.1196016.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929836" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Carbachol/pharmacology ; Epithelium/embryology/innervation ; Ganglia, Parasympathetic/cytology/embryology/*physiology ; Humans ; Keratin-5/analysis ; Lung/embryology ; Male ; Mice ; Morphogenesis ; Multipotent Stem Cells/cytology/*physiology ; Neurons/*physiology ; Organogenesis ; Prostate/embryology ; Regeneration ; Submandibular Gland/cytology/*embryology/*innervation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Cell type-specific loss of BDNF signaling mimics optogenetic control of cocaine reward (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: The nucleus accumbens is a key mediator of cocaine reward, but the distinct roles of the two subpopulations of nucleus accumbens projection neurons, those expressing dopamine D1 versus D2 receptors, are poorly understood. We show that deletion of TrkB, the brain-derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine reward. Because loss of TrkB in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on cocaine reward. Activation of D2+ neurons, mimicking the loss of TrkB, suppresses cocaine reward, with opposite effects induced by activation of D1+ neurons. These results provide insight into the molecular control of D1+ and D2+ neuronal activity as well as the circuit-level contribution of these cell types to cocaine reward.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011229/" 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/PMC3011229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobo, Mary Kay -- Covington, Herbert E 3rd -- Chaudhury, Dipesh -- Friedman, Allyson K -- Sun, HaoSheng -- Damez-Werno, Diane -- Dietz, David M -- Zaman, Samir -- Koo, Ja Wook -- Kennedy, Pamela J -- Mouzon, Ezekiell -- Mogri, Murtaza -- Neve, Rachael L -- Deisseroth, Karl -- Han, Ming-Hu -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-20/DA/NIDA NIH HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA014133-10/DA/NIDA NIH HHS/ -- R01 DA014133-11/DA/NIDA NIH HHS/ -- R01 DA014133-12/DA/NIDA NIH HHS/ -- R01 MH051399/MH/NIMH NIH HHS/ -- R01 MH051399-19/MH/NIMH NIH HHS/ -- R01 MH051399-20/MH/NIMH NIH HHS/ -- T32 DA007135-26A2/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):385-90. doi: 10.1126/science.1188472.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/*metabolism ; Cocaine/*pharmacology ; Cocaine-Related Disorders/*metabolism ; Conditioning (Psychology) ; Light ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Models, Biological ; Motor Activity/drug effects ; Neurons/*metabolism ; Nucleus Accumbens/cytology/*metabolism ; RNA, Messenger/genetics/metabolism ; Receptor, trkB/genetics/*metabolism ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; *Reward ; Rhodopsin/genetics/metabolism ; *Signal Transduction
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    Cell biology. Gett'N-WASP stripes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gautel, Mathias -- Ehler, Elisabeth -- New York, N.Y. -- Science. 2010 Dec 10;330(6010):1491-2. doi: 10.1126/science.1199920.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉King's College London British Heart Foundation Centre of Research Excellence, Cardiovascular Division, London, SE1 1UL, UK. mathias.gautel@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21148382" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actins/*metabolism ; Animals ; Connectin ; Insulin-Like Growth Factor I/*metabolism ; Mice ; Muscle Development ; Muscle Proteins/chemistry/*metabolism ; Protein Kinases/metabolism ; Sarcomeres/*metabolism/ultrastructure ; Wiskott-Aldrich Syndrome Protein, Neuronal/chemistry/*metabolism ; src Homology Domains
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  • 17
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-02
    Description: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
    Print ISSN: 0036-8075
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    Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manicassamy, Santhakumar -- Reizis, Boris -- Ravindran, Rajesh -- Nakaya, Helder -- Salazar-Gonzalez, Rosa Maria -- Wang, Yi-Chong -- Pulendran, Bali -- HHSN266 200700006C/PHS HHS/ -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI056499/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01DK057665,/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638,/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266,/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):849-53. doi: 10.1126/science.1188510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Dendritic Cells/*immunology/metabolism ; Gene Expression Profiling ; *Inflammation ; Inflammatory Bowel Diseases/*immunology ; Intestinal Mucosa/cytology/*immunology/metabolism ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Tretinoin/metabolism ; Wnt Proteins/metabolism ; beta Catenin/*metabolism
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    Immunology. Have you seen your mother, baby (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Betz, Alexander G -- MC_U105184296/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1635-6. doi: 10.1126/science.1200406.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Protein & Nucleic Acid Chemistry Facility, University of Cambridge, Cambridge CB2 0QH, UK. betz@mrc-lmb.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/embryology/immunology/physiology ; Cell Lineage ; Fetal Development ; Fetus/*immunology ; Forkhead Transcription Factors/analysis/genetics ; Hematopoietic Stem Cells/*physiology ; Humans ; *Immune Tolerance ; Liver/embryology/immunology/physiology ; Lymphopoiesis ; Mice ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/*immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Medicine. The microbes made me eat it (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandoval, Darleen A -- Seeley, Randy J -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):179-80. doi: 10.1126/science.1188876.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolic Diseases Institute and Department of Internal Medicine, University of Cincinnati, Cincinnati, OH 45237, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Physiological Phenomena ; Body Weight ; Disease Susceptibility ; Humans ; Immune System/*physiology ; Intestines/*microbiology ; Metabolic Syndrome X/*etiology/immunology/microbiology ; Mice ; Obesity/*etiology/immunology/microbiology ; Toll-Like Receptor 5/deficiency/genetics/*metabolism
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    Research funding. Politics and parthenotes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tingen, C -- Rodriguez, S -- Campo-Engelstein, L -- Woodruff, T K -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):453. doi: 10.1126/science.1196881.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo Research/*legislation & jurisprudence ; *Embryonic Stem Cells ; Female ; Financing, Government/legislation & jurisprudence ; Humans ; Mice ; Ovum/physiology ; *Parthenogenesis ; Research Support as Topic/*legislation & jurisprudence ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Intestinal stem cell replacement follows a pattern of neutral drift (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: With the capacity for rapid self-renewal and regeneration, the intestinal epithelium is stereotypical of stem cell-supported tissues. Yet the pattern of stem cell turnover remains in question. Applying analytical methods from population dynamics and statistical physics to an inducible genetic labeling system, we showed that clone size distributions conform to a distinctive scaling behavior at short times. This result demonstrates that intestinal stem cells form an equipotent population in which the loss of a stem cell is compensated by the multiplication of a neighbor, leading to neutral drift dynamics in which clones expand and contract at random until they either take over the crypt or they are lost. Combined with long-term clonal fate data, we show that the rate of stem cell replacement is comparable to the cell division rate, implying that neutral drift and symmetrical cell divisions are central to stem cell homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Garcia, Carlos -- Klein, Allon M -- Simons, Benjamin D -- Winton, Douglas J -- G0800784/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):822-5. doi: 10.1126/science.1196236. Epub 2010 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Division ; Cell Lineage ; Clone Cells/cytology ; Colon/cytology ; Homeostasis ; Intestinal Mucosa/*cytology ; Intestine, Small/cytology ; Mice ; Stem Cells/*cytology/physiology
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    Medicine. The blood stem cell Holy Grail? (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sauvageau, Guy -- Humphries, R Keith -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1291-2. doi: 10.1126/science.1195173.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Stem Cells Laboratory, Institute of Research in Immunology and Cancer, University of Montreal, Montreal, QC H3C 3J7, Canada. guy.sauvageau@umontreal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Fetal Blood/cytology ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/*drug effects/physiology ; Humans ; Mice ; Purines/chemistry/metabolism/*pharmacology ; Receptors, Aryl Hydrocarbon/*antagonists & inhibitors/metabolism ; Small Molecule Libraries ; Species Specificity
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    Developmental biology. Microenvironment mimicry (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhatia, Mickie -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1024-5. doi: 10.1126/science.1194919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell and Cancer Research Institute, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. mbhatia@mcmaster.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/*methods ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Elasticity ; Humans ; Hydrogels ; Mice ; Muscle Fibers, Skeletal/*cytology/physiology ; Myoblasts, Skeletal/cytology/physiology ; Regeneration ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/*physiology
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    Identification of a cell of origin for human prostate cancer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: Luminal cells are believed to be the cells of origin for human prostate cancer, because the disease is characterized by luminal cell expansion and the absence of basal cells. Yet functional studies addressing the origin of human prostate cancer have not previously been reported because of a lack of relevant in vivo human models. Here we show that basal cells from primary benign human prostate tissue can initiate prostate cancer in immunodeficient mice. The cooperative effects of AKT, ERG, and androgen receptor in basal cells recapitulated the histological and molecular features of human prostate cancer, with loss of basal cells and expansion of luminal cells expressing prostate-specific antigen and alpha-methylacyl-CoA racemase. Our results demonstrate that histological characterization of cancers does not necessarily correlate with the cellular origins of the disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917982/" 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/PMC2917982/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldstein, Andrew S -- Huang, Jiaoti -- Guo, Changyong -- Garraway, Isla P -- Witte, Owen N -- GM07185/GM/NIGMS NIH HHS/ -- P50 CA092131/CA/NCI NIH HHS/ -- P50 CA092131-06/CA/NCI NIH HHS/ -- T32 GM007185/GM/NIGMS NIH HHS/ -- T32 GM007185-35/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):568-71. doi: 10.1126/science.1189992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/metabolism ; Cell Separation ; *Cell Transformation, Neoplastic ; Epithelial Cells/metabolism/*pathology ; Epithelium/pathology ; Flow Cytometry ; Humans ; Keratins/analysis ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Prostate/cytology/metabolism/*pathology ; Prostatic Intraepithelial Neoplasia/metabolism/*pathology ; Prostatic Neoplasms/metabolism/*pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Androgen/metabolism ; Trans-Activators/metabolism ; Transduction, Genetic
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    Evidence for an alternative glycolytic pathway in rapidly proliferating cells (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: Proliferating cells, including cancer cells, require altered metabolism to efficiently incorporate nutrients such as glucose into biomass. The M2 isoform of pyruvate kinase (PKM2) promotes the metabolism of glucose by aerobic glycolysis and contributes to anabolic metabolism. Paradoxically, decreased pyruvate kinase enzyme activity accompanies the expression of PKM2 in rapidly dividing cancer cells and tissues. We demonstrate that phosphoenolpyruvate (PEP), the substrate for pyruvate kinase in cells, can act as a phosphate donor in mammalian cells because PEP participates in the phosphorylation of the glycolytic enzyme phosphoglycerate mutase (PGAM1) in PKM2-expressing cells. We used mass spectrometry to show that the phosphate from PEP is transferred to the catalytic histidine (His11) on human PGAM1. This reaction occurred at physiological concentrations of PEP and produced pyruvate in the absence of PKM2 activity. The presence of histidine-phosphorylated PGAM1 correlated with the expression of PKM2 in cancer cell lines and tumor tissues. Thus, decreased pyruvate kinase activity in PKM2-expressing cells allows PEP-dependent histidine phosphorylation of PGAM1 and may provide an alternate glycolytic pathway that decouples adenosine triphosphate production from PEP-mediated phosphotransfer, allowing for the high rate of glycolysis to support the anabolic metabolism observed in many proliferating cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030121/" 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/PMC3030121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vander Heiden, Matthew G -- Locasale, Jason W -- Swanson, Kenneth D -- Sharfi, Hadar -- Heffron, Greg J -- Amador-Noguez, Daniel -- Christofk, Heather R -- Wagner, Gerhard -- Rabinowitz, Joshua D -- Asara, John M -- Cantley, Lewis C -- 1K08CA136983/CA/NCI NIH HHS/ -- 1P01CA120964-01A/CA/NCI NIH HHS/ -- 5 T32 CA009361-28/CA/NCI NIH HHS/ -- 5P30CA006516-43/CA/NCI NIH HHS/ -- K08 CA136983/CA/NCI NIH HHS/ -- K08 CA136983-02/CA/NCI NIH HHS/ -- P01 CA089021/CA/NCI NIH HHS/ -- P01 CA089021-10/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-01A1/CA/NCI NIH HHS/ -- P01 GM047467/GM/NIGMS NIH HHS/ -- P01 GM047467-20/GM/NIGMS NIH HHS/ -- P01CA089021/CA/NCI NIH HHS/ -- P01GM047467/GM/NIGMS NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30 CA006516-43S1/CA/NCI NIH HHS/ -- R01 AI078063/AI/NIAID NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01-GM56302/GM/NIGMS NIH HHS/ -- R21 CA128620/CA/NCI NIH HHS/ -- R21/R33 DK070299/DK/NIDDK NIH HHS/ -- R33 DK070299/DK/NIDDK NIH HHS/ -- R33 DK070299-03/DK/NIDDK NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA009361/CA/NCI NIH HHS/ -- T32 CA009361-28/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1492-9. doi: 10.1126/science.1188015.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847263" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Female ; Glucose/*metabolism ; Glyceric Acids/metabolism ; *Glycolysis ; Histidine/metabolism ; Humans ; Isoenzymes/metabolism ; Kinetics ; Male ; Mammary Neoplasms, Animal/metabolism ; Mice ; Neoplasms/*metabolism/pathology ; Phosphoenolpyruvate/metabolism ; Phosphoglycerate Mutase/*metabolism ; Phosphopyruvate Hydratase/metabolism ; Phosphorylation ; Prostatic Neoplasms/metabolism ; Pyruvate Kinase/*metabolism ; Pyruvic Acid/metabolism ; Recombinant Proteins/metabolism
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    Cyclooxygenase-2 controls energy homeostasis in mice by de novo recruitment of brown adipocytes (2010)
    American Association for the Advancement of Science (AAAS)
    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
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    Immunology. Innate lymphoid cell relations (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veldhoen, Marc -- Withers, David R -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):594-5. doi: 10.1126/science.1198298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Lymphocyte Signalling and Development, Babraham Institute, Cambridge CB22 3AT, UK. marc.veldhoen@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030634" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Cell Differentiation ; *Cell Lineage ; Fetus/cytology/immunology/metabolism ; Intestines/embryology/*immunology/microbiology ; Liver/cytology/immunology ; Lymphocyte Subsets/cytology/*immunology/metabolism ; Lymphocytes/cytology/*immunology/metabolism ; Lymphoid Progenitor Cells/*cytology ; Lymphoid Tissue/cytology/immunology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism
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    G protein subunit Galpha13 binds to integrin alphaIIbbeta3 and mediates integrin "outside-in" signaling (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-16
    Description: Integrins mediate cell adhesion to the extracellular matrix and transmit signals within the cell that stimulate cell spreading, retraction, migration, and proliferation. The mechanism of integrin outside-in signaling has been unclear. We found that the heterotrimeric guanine nucleotide-binding protein (G protein) Galpha13 directly bound to the integrin beta3 cytoplasmic domain and that Galpha13-integrin interaction was promoted by ligand binding to the integrin alphaIIbbeta3 and by guanosine triphosphate (GTP) loading of Galpha13. Interference of Galpha13 expression or a myristoylated fragment of Galpha13 that inhibited interaction of alphaIIbbeta3 with Galpha13 diminished activation of protein kinase c-Src and stimulated the small guanosine triphosphatase RhoA, consequently inhibiting cell spreading and accelerating cell retraction. We conclude that integrins are noncanonical Galpha13-coupled receptors that provide a mechanism for dynamic regulation of RhoA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842917/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Haixia -- Shen, Bo -- Flevaris, Panagiotis -- Chow, Christina -- Lam, Stephen C-T -- Voyno-Yasenetskaya, Tatyana A -- Kozasa, Tohru -- Du, Xiaoping -- GM061454/GM/NIGMS NIH HHS/ -- GM074001/GM/NIGMS NIH HHS/ -- HL062350/HL/NHLBI NIH HHS/ -- HL068819/HL/NHLBI NIH HHS/ -- HL080264/HL/NHLBI NIH HHS/ -- R01 GM061454/GM/NIGMS NIH HHS/ -- R01 GM061454-09/GM/NIGMS NIH HHS/ -- R01 GM074001/GM/NIGMS NIH HHS/ -- R01 GM074001-02/GM/NIGMS NIH HHS/ -- R01 HL062350/HL/NHLBI NIH HHS/ -- R01 HL062350-09/HL/NHLBI NIH HHS/ -- R01 HL068819/HL/NHLBI NIH HHS/ -- R01 HL068819-08/HL/NHLBI NIH HHS/ -- R01 HL080264/HL/NHLBI NIH HHS/ -- R01 HL080264-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):340-3. doi: 10.1126/science.1174779.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Illinois at Chicago, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Blood Platelets/*physiology ; Clot Retraction ; Fibrinogen/metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/genetics/*metabolism ; Humans ; Integrin beta3/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Platelet Adhesiveness ; Platelet Glycoprotein GPIIb-IIIa Complex/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; rhoA GTP-Binding Protein/antagonists & inhibitors/metabolism
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    Lineage relationship analysis of RORgammat+ innate lymphoid cells (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Lymphoid tissue-inducer (LTi) cells initiate the development of lymphoid tissues through the activation of local stromal cells in a process similar to inflammation. LTi cells express the nuclear hormone receptor RORgammat, which also directs the expression of the proinflammatory cytokine interleukin-17 in T cells. We show here that LTi cells are part of a larger family of proinflammatory RORgammat(+) innate lymphoid cells (ILCs) that differentiate from distinct fetal liver RORgammat(+) precursors. The fate of RORgammat(+) ILCs is determined by mouse age, and after birth, favors the generation of cells involved in intestinal homeostasis and defense. Contrary to RORgammat(+) T cells, however, RORgammat(+) ILCs develop in the absence of microbiota. Our study indicates that RORgammat(+) ILCs evolve to preempt intestinal colonization by microbial symbionts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawa, Shinichiro -- Cherrier, Marie -- Lochner, Matthias -- Satoh-Takayama, Naoko -- Fehling, Hans Jorg -- Langa, Francina -- Di Santo, James P -- Eberl, Gerard -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):665-9. doi: 10.1126/science.1194597. Epub 2010 Sep 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphoid Tissue Development Unit, Institut Pasteur, 75724 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929731" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Adoptive Transfer ; Animals ; Bacterial Physiological Phenomena ; Cell Differentiation ; Cell Lineage ; Fetus/cytology/immunology/metabolism ; Homeostasis ; Immunity, Mucosal ; Intestinal Mucosa/*immunology ; Intestine, Small/embryology/*immunology/microbiology ; Liver/cytology/embryology/immunology ; Lymphocyte Subsets/cytology/*immunology/metabolism ; Lymphocytes/cytology/*immunology/metabolism ; Lymphoid Progenitor Cells/*cytology ; Lymphoid Tissue/cytology/immunology ; Lymphopoiesis ; Mice ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 3/*metabolism ; Receptors, CCR6/metabolism ; Symbiosis ; T-Lymphocyte Subsets/cytology/immunology/metabolism
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    Meiotic recombination provokes functional activation of the p53 regulatory network (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: The evolutionary appearance of p53 protein probably preceded its role in tumor suppression, suggesting that there may be unappreciated functions for this protein. Using genetic reporters as proxies to follow in vivo activation of the p53 network in Drosophila, we discovered that the process of meiotic recombination instigates programmed activation of p53 in the germ line. Specifically, double-stranded breaks in DNA generated by the topoisomerase Spo11 provoked functional p53 activity, which was prolonged in cells defective for meiotic DNA repair. This intrinsic stimulus for the p53 regulatory network is highly conserved because Spo11-dependent activation of p53 also occurs in mice. Our findings establish a physiological role for p53 in meiosis and suggest that tumor-suppressive functions may have been co-opted from primordial activities linked to recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917750/" 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/PMC2917750/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Wan-Jin -- Chapo, Joseph -- Roig, Ignasi -- Abrams, John M -- R01 AA017328/AA/NIAAA NIH HHS/ -- R01 AA017328-03/AA/NIAAA NIH HHS/ -- R01 AA017328-04/AA/NIAAA NIH HHS/ -- R01 GM072124/GM/NIGMS NIH HHS/ -- R01 GM072124-10/GM/NIGMS NIH HHS/ -- R01 GM072124-11/GM/NIGMS NIH HHS/ -- R01 GM072124-12/GM/NIGMS NIH HHS/ -- R01 GM072124-13/GM/NIGMS NIH HHS/ -- R01 GM072124-14A1/GM/NIGMS NIH HHS/ -- R01 GM072124-15/GM/NIGMS NIH HHS/ -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-09/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- R01AA017328/AA/NIAAA NIH HHS/ -- R01GM072124/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1278-81. doi: 10.1126/science.1185640.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; DNA/genetics/metabolism ; DNA Breaks, Double-Stranded ; DNA Damage ; DNA Helicases ; DNA Repair ; DNA Topoisomerases, Type II/genetics/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Egg Proteins/genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Endodeoxyribonucleases ; Esterases/genetics/metabolism ; Female ; Gene Expression Regulation, Developmental ; *Gene Regulatory Networks ; Genes, Insect ; *Genes, p53 ; Germ Cells/metabolism ; Male ; *Meiosis ; Mice ; Mice, Knockout ; Oogenesis ; *Recombination, Genetic ; Spermatocytes/physiology ; Tumor Suppressor Protein p53/genetics/*metabolism ; Ultraviolet Rays
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    Linear arrays of nuclear envelope proteins harness retrograde actin flow for nuclear movement (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: Nuclei move to specific locations to polarize migrating and differentiating cells. Many nuclear movements are microtubule-dependent. However, nuclear movement to reorient the centrosome in migrating fibroblasts occurs through an unknown actin-dependent mechanism. We found that linear arrays of outer (nesprin2G) and inner (SUN2) nuclear membrane proteins assembled on and moved with retrogradely moving dorsal actin cables during nuclear movement in polarizing fibroblasts. Inhibition of nesprin2G, SUN2, or actin prevented nuclear movement and centrosome reorientation. The coupling of actin cables to the nuclear membrane for nuclear movement via specific membrane proteins indicates that, like plasma membrane integrins, nuclear membrane proteins assemble into actin-dependent arrays for force transduction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3938394/" 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/PMC3938394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luxton, G W Gant -- Gomes, Edgar R -- Folker, Eric S -- Vintinner, Erin -- Gundersen, Gregg G -- GM06929/GM/NIGMS NIH HHS/ -- NS059352/NS/NINDS NIH HHS/ -- R01 GM062939/GM/NIGMS NIH HHS/ -- R01 GM099481/GM/NIGMS NIH HHS/ -- R01 NS059352/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):956-9. doi: 10.1126/science.1189072.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724637" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Animals ; Cell Movement/physiology ; Cell Nucleus/*metabolism ; Centrosome/physiology ; Fibroblasts ; Lysophospholipids/metabolism ; Membrane Proteins/metabolism ; Mice ; Movement ; NIH 3T3 Cells ; Nerve Tissue Proteins/metabolism ; Nuclear Envelope/*metabolism ; Nuclear Proteins/*metabolism ; Telomere-Binding Proteins/metabolism
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    Mcl-1 is essential for germinal center formation and B cell memory (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Lymphocyte survival during immune responses is controlled by the relative expression of pro- and anti-apoptotic molecules, regulating the magnitude, quality, and duration of the response. We investigated the consequences of deleting genes encoding the anti-apoptotic molecules Mcl1 and Bcl2l1 (Bcl-x(L)) from B cells using an inducible system synchronized with expression of activation-induced cytidine deaminase (Aicda) after immunization. This revealed Mcl1 and not Bcl2l1 to be indispensable for the formation and persistence of germinal centers (GCs). Limiting Mcl1 expression reduced the magnitude of the GC response with an equivalent, but not greater, effect on memory B cell formation and no effect on persistence. Our results identify Mcl1 as the main anti-apoptotic regulator of activated B cell survival and suggest distinct mechanisms controlling survival of GC and memory B cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991396/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vikstrom, Ingela -- Carotta, Sebastian -- Luthje, Katja -- Peperzak, Victor -- Jost, Philipp J -- Glaser, Stefan -- Busslinger, Meinrad -- Bouillet, Philippe -- Strasser, Andreas -- Nutt, Stephen L -- Tarlinton, David M -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1095-9. doi: 10.1126/science.1191793. Epub 2010 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; B-Lymphocytes/*immunology ; Cell Survival ; Gene Deletion ; Germinal Center/cytology/*immunology ; *Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2/genetics/*immunology ; bcl-X Protein/genetics/immunology
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    Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5 (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-06
    Description: Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota, and transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714868/" 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/PMC4714868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vijay-Kumar, Matam -- Aitken, Jesse D -- Carvalho, Frederic A -- Cullender, Tyler C -- Mwangi, Simon -- Srinivasan, Shanthi -- Sitaraman, Shanthi V -- Knight, Rob -- Ley, Ruth E -- Gewirtz, Andrew T -- DK061417/DK/NIDDK NIH HHS/ -- DK06439/DK/NIDDK NIH HHS/ -- DK083275/DK/NIDDK NIH HHS/ -- K01 DK083275/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):228-31. doi: 10.1126/science.1179721. Epub 2010 Mar 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Emory University, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Physiological Phenomena ; Blood Glucose/analysis ; Body Fat Distribution ; Body Weight ; Caloric Restriction ; Dietary Fats/administration & dosage ; Female ; Germ-Free Life ; Hyperphagia/etiology ; *Immunity, Innate ; Insulin Resistance ; Intestinal Mucosa/immunology ; Intestines/*microbiology ; Male ; Metabolic Syndrome X/*etiology/immunology/microbiology ; Mice ; Mice, Knockout ; Obesity/etiology/immunology/microbiology/prevention & control ; Toll-Like Receptor 5/deficiency/genetics/*metabolism
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    Btbd7 regulates epithelial cell dynamics and branching morphogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: During embryonic development, many organs form by extensive branching of epithelia through the formation of clefts and buds. In cleft formation, buds are delineated by the conversion of epithelial cell-cell adhesions to cell-matrix adhesions, but the mechanisms of cleft formation are not clear. We have identified Btbd7 as a dynamic regulator of branching morphogenesis. Btbd7 provides a mechanistic link between the extracellular matrix and cleft propagation through its highly focal expression leading to local regulation of Snail2 (Slug), E-cadherin, and epithelial cell motility. Inhibition experiments show that Btbd7 is required for branching of embryonic mammalian salivary glands and lungs. Hence, Btbd7 is a regulatory gene that promotes epithelial tissue remodeling and formation of branched organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412157/" 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/PMC3412157/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Onodera, Tomohiro -- Sakai, Takayoshi -- Hsu, Jeff Chi-feng -- Matsumoto, Kazue -- Chiorini, John A -- Yamada, Kenneth M -- ZIA DE000525-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):562-5. doi: 10.1126/science.1191880.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cadherins/metabolism ; Cell Adhesion ; Cell Line ; Cell Movement ; Dogs ; Epithelial Cells/*physiology ; Fibronectins/genetics/metabolism ; Genes, Regulator ; Lung/*embryology/metabolism ; Mice ; Mice, Inbred ICR ; Models, Biological ; Molecular Sequence Data ; *Morphogenesis ; Nuclear Proteins ; Organ Culture Techniques ; Proteins/chemistry/*genetics/*physiology ; RNA, Small Interfering ; Salivary Glands/*embryology/metabolism ; Submandibular Gland/embryology ; Transcription Factors/genetics/metabolism ; Transfection
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    Prdm9 controls activation of mammalian recombination hotspots (2010)
    American Association for the Advancement of Science (AAAS)
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    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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    Platelets amplify inflammation in arthritis via collagen-dependent microparticle production (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: In addition to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory responses. We investigated the role of platelets in the autoimmune disease rheumatoid arthritis. We identified platelet microparticles--submicrometer vesicles elaborated by activated platelets--in joint fluid from patients with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1. Consistent with these findings, depletion of platelets attenuated murine inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927861/" 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/PMC2927861/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boilard, Eric -- Nigrovic, Peter A -- Larabee, Katherine -- Watts, Gerald F M -- Coblyn, Jonathan S -- Weinblatt, Michael E -- Massarotti, Elena M -- Remold-O'Donnell, Eileen -- Farndale, Richard W -- Ware, Jerry -- Lee, David M -- G0500707/Medical Research Council/United Kingdom -- HL091269/HL/NHLBI NIH HHS/ -- HL50545/HL/NHLBI NIH HHS/ -- K08AR051321/AR/NIAMS NIH HHS/ -- P01 AI065858/AI/NIAID NIH HHS/ -- R01 HL050545/HL/NHLBI NIH HHS/ -- R01 HL050545-16/HL/NHLBI NIH HHS/ -- R01 HL050545-18/HL/NHLBI NIH HHS/ -- R21 HL091269/HL/NHLBI NIH HHS/ -- R21 HL091269-01A2/HL/NHLBI NIH HHS/ -- RG/09/003/27122/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):580-3. doi: 10.1126/science.1181928.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/blood/immunology ; Arthritis, Rheumatoid/*blood/*immunology/physiopathology ; Blood Platelets/cytology/*physiology/ultrastructure ; Cell-Derived Microparticles/metabolism/*physiology ; Cells, Cultured ; Collagen/*metabolism ; Cytokines/*metabolism ; Extracellular Matrix/metabolism ; Fibroblasts/immunology/metabolism ; Humans ; Interleukin-1/metabolism ; Mice ; Mice, Transgenic ; Platelet Activation ; Platelet Membrane Glycoproteins/metabolism ; Receptors, Collagen/metabolism ; Synovial Fluid/cytology/*immunology ; Synovial Membrane/cytology/immunology
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    Cancer. Targeting bacteria to improve cancer therapy (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, Anand G -- Kaufmann, Scott H -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):766-7. doi: 10.1126/science.1198310.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents, Phytogenic/administration & dosage/*metabolism/toxicity ; Bacteria/drug effects/enzymology ; Camptothecin/administration & dosage/*analogs & derivatives/metabolism/toxicity ; Drug Evaluation, Preclinical ; Enzyme Inhibitors/*pharmacology ; Escherichia coli/drug effects/enzymology ; Glucuronidase/*antagonists & inhibitors ; Intestinal Mucosa/drug effects/metabolism/*microbiology ; Mice
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    Male mice not alone in research (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolon, Brad -- Barthold, Stephen W -- Boyd, Kelli L -- Brayton, Cory -- Cardiff, Robert D -- Cork, Linda C -- Eaton, Kathryn A -- Schoeb, Trenton R -- Sundberg, John P -- Ward, Jerrold M -- U01 CA141582/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1103. doi: 10.1126/science.328.5982.1103-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508110" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Experimentation ; Animals ; Bias (Epidemiology) ; *Biomedical Research ; Female ; Male ; Mice ; *Models, Animal ; Sex Characteristics
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    Sex-specific parent-of-origin allelic expression in the mouse brain (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Genomic imprinting results in preferential gene expression from paternally versus maternally inherited chromosomes. We used a genome-wide approach to uncover sex-specific parent-of-origin allelic effects in the adult mouse brain. Our study identified preferential selection of the maternally inherited X chromosome in glutamatergic neurons of the female cortex. Moreover, analysis of the cortex and hypothalamus identified 347 autosomal genes with sex-specific imprinting features. In the hypothalamus, sex-specific imprinted genes were mostly found in females, which suggests parental influence over the hypothalamic function of daughters. We show that interleukin-18, a gene linked to diseases with sex-specific prevalence, is subject to complex, regional, and sex-specific parental effects in the brain. Parent-of-origin effects thus provide new avenues for investigation of sexual dimorphism in brain function and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997643/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- Zhang, Jiangwen -- Butler, James E -- Haig, David -- Dulac, Catherine -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):682-5. doi: 10.1126/science.1190831. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616234" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Crosses, Genetic ; Dioxygenases ; *Epigenesis, Genetic ; Female ; Gene Expression Profiling ; *Genes, X-Linked ; *Genomic Imprinting ; Glutamic Acid/metabolism ; Interleukin-18/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Neurons/metabolism ; Oxygenases/genetics ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/cytology/*metabolism ; Preoptic Area/cytology/*metabolism ; Ribosomal Proteins/genetics ; *Sex Characteristics ; Succinate Dehydrogenase/genetics ; X Chromosome Inactivation
    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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  • 41
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    Eppendorf winner. Parental control over the brain (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):770-1. doi: 10.1126/science.1199054.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. cgregg@MCB.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051625" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Awards and Prizes ; *Fathers ; *Gene Expression ; Gene Expression Profiling ; *Genomic Imprinting ; Humans ; Interleukin-18 ; Mice ; Mice, Inbred C57BL ; *Mothers ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/embryology/growth & development/*metabolism ; Preoptic Area/embryology/growth & development/*metabolism ; Sex Characteristics
    Print ISSN: 0036-8075
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  • 42
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    Requirement of prorenin receptor and vacuolar H+-ATPase-mediated acidification for Wnt signaling (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: Wnt/beta-catenin signaling is important in stem cell biology, embryonic development, and disease, including cancer. However, the mechanism of Wnt signal transmission, notably how the receptors are activated, remains incompletely understood. We found that the prorenin receptor (PRR) is a component of the Wnt receptor complex. PRR functions in a renin-independent manner as an adaptor between Wnt receptors and the vacuolar H+-adenosine triphosphatase (V-ATPase) complex. Moreover, PRR and V-ATPase were required to mediate Wnt signaling during antero-posterior patterning of Xenopus early central nervous system development. The results reveal an unsuspected role for the prorenin receptor, V-ATPase activity, and acidification during Wnt/beta-catenin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruciat, Cristina-Maria -- Ohkawara, Bisei -- Acebron, Sergio P -- Karaulanov, Emil -- Reinhard, Carmen -- Ingelfinger, Dierk -- Boutros, Michael -- Niehrs, Christof -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):459-63. doi: 10.1126/science.1179802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Embryology, DKFZ-ZMBH Alliance, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Cell Line ; Cell Line, Tumor ; Central Nervous System/cytology/embryology ; Embryo, Nonmammalian/metabolism ; Frizzled Receptors/metabolism ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics/metabolism ; Humans ; Hydrogen-Ion Concentration ; LDL-Receptor Related Proteins/metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Phosphorylation ; RNA, Small Interfering ; Receptors, Cell Surface/genetics/*metabolism ; *Signal Transduction ; Vacuolar Proton-Translocating ATPases/antagonists & inhibitors/*metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Xenopus/embryology/metabolism ; Xenopus Proteins/genetics/*metabolism ; beta Catenin/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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  • 43
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    High-resolution analysis of parent-of-origin allelic expression in the mouse brain (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Genomic imprinting results in preferential expression of the paternal or maternal allele of certain genes. We have performed a genome-wide characterization of imprinting in the mouse embryonic and adult brain. This approach uncovered parent-of-origin allelic effects of more than 1300 loci. We identified parental bias in the expression of individual genes and of specific transcript isoforms, with differences between brain regions. Many imprinted genes are expressed in neural systems associated with feeding and motivated behaviors, and parental biases preferentially target genetic pathways governing metabolism and cell adhesion. We observed a preferential maternal contribution to gene expression in the developing brain and a major paternal contribution in the adult brain. Thus, parental expression bias emerges as a major mode of epigenetic regulation in the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005244/" 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/PMC3005244/" 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 -- Weissbourd, Brandon -- Luo, Shujun -- Schroth, Gary P -- Haig, David -- Dulac, Catherine -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):643-8. doi: 10.1126/science.1190830. Epub 2010 Jul 8.〈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/20616232" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Behavior, Animal ; Brain/*embryology/growth & development/*metabolism ; Epigenesis, Genetic ; Fathers ; Female ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Silencing ; *Genomic Imprinting ; Male ; Mice ; Mothers ; Multigene Family ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/embryology/growth & development/metabolism ; Preoptic Area/embryology/growth & development/metabolism ; Sex Characteristics
    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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  • 44
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    Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: Stem cells that naturally reside in adult tissues, such as muscle stem cells (MuSCs), exhibit robust regenerative capacity in vivo that is rapidly lost in culture. Using a bioengineered substrate to recapitulate key biophysical and biochemical niche features in conjunction with a highly automated single-cell tracking algorithm, we show that substrate elasticity is a potent regulator of MuSC fate in culture. Unlike MuSCs on rigid plastic dishes (approximately 10(6) kilopascals), MuSCs cultured on soft hydrogel substrates that mimic the elasticity of muscle (12 kilopascals) self-renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into mice and assayed histologically and quantitatively by noninvasive bioluminescence imaging. Our studies provide novel evidence that by recapitulating physiological tissue rigidity, propagation of adult muscle stem cells is possible, enabling future cell-based therapies for muscle-wasting diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, P M -- Havenstrite, K L -- Magnusson, K E G -- Sacco, A -- Leonardi, N A -- Kraft, P -- Nguyen, N K -- Thrun, S -- Lutolf, M P -- Blau, H M -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- 52005886/Howard Hughes Medical Institute/ -- AG009521/AG/NIA NIH HHS/ -- AG020961/AG/NIA NIH HHS/ -- CA09151/CA/NCI NIH HHS/ -- HL096113/HL/NHLBI NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG020961/AG/NIA NIH HHS/ -- R01 AG020961-06A2/AG/NIA NIH HHS/ -- R01 AG020961-07/AG/NIA NIH HHS/ -- R01 HL096113/HL/NHLBI NIH HHS/ -- R01 HL096113-03/HL/NHLBI NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA009151-35/CA/NCI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32 HD007249-25/HD/NICHD NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- U01 HL100397-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1078-81. doi: 10.1126/science.1191035. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647425" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Count ; Cell Culture Techniques/*methods ; Cell Death ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Separation ; Cell Survival ; Cells, Cultured ; Elastic Modulus ; Hydrogels ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Muscle Fibers, Skeletal/*cytology/physiology ; Muscle, Skeletal/*cytology ; Polyethylene Glycols ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/cytology/*physiology
    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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  • 45
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    Stem cells. Reprogrammed cells come up short, for now (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1191. doi: 10.1126/science.327.5970.1191.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Embryonic Stem Cells/cytology/*physiology ; Humans ; Induced Pluripotent Stem Cells/cytology/*physiology ; Mice ; Neurogenesis ; Neuroglia/cytology ; Neurons/cytology
    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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  • 46
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    Loss of Rap1 induces telomere recombination in the absence of NHEJ or a DNA damage signal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Shelterin is an essential telomeric protein complex that prevents DNA damage signaling and DNA repair at mammalian chromosome ends. Here we report on the role of the TRF2-interacting factor Rap1, a conserved shelterin subunit of unknown function. We removed Rap1 from mouse telomeres either through gene deletion or by replacing TRF2 with a mutant that does not bind Rap1. Rap1 was dispensable for the essential functions of TRF2--repression of ATM kinase signaling and nonhomologous end joining (NHEJ)--and mice lacking telomeric Rap1 were viable and fertile. However, Rap1 was critical for the repression of homology-directed repair (HDR), which can alter telomere length. The data reveal that HDR at telomeres can take place in the absence of DNA damage foci and underscore the functional compartmentalization within shelterin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- Kabir, Shaheen -- van Overbeek, Megan -- Celli, Giulia B -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1657-61. doi: 10.1126/science.1185100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339076" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Checkpoint Kinase 2 ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Gene Deletion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Recombination, Genetic ; Signal Transduction ; Sister Chromatid Exchange ; Telomere/*genetics/metabolism ; Telomere-Binding Proteins/chemistry/*genetics/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
    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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  • 47
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    Cell biology. Puzzled by PML (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culjkovic-Kraljacic, Bijana -- Borden, Katherine L B -- R01 CA080728/CA/NCI NIH HHS/ -- R01 CA098571/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1183-4. doi: 10.1126/science.1199405.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Research in Immunology and Cancer, Department of Pathology and Cell Biology, Universite de Montreal, Pavillion Marcelle-Coutu, Chemin Polytechnique, Montreal, QC, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Calcium/*metabolism ; *Calcium Signaling ; Endoplasmic Reticulum/*metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Intranuclear Space/metabolism ; Mice ; Mitochondria/metabolism ; Nuclear Proteins/*metabolism ; Phosphorylation ; Protein Isoforms/metabolism ; Transcription Factors/*metabolism ; Tumor Suppressor Proteins/*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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    Cancer. Awakening immunity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schreiber, Hans -- Rowley, Donald A -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):761-2. doi: 10.1126/science.1198345.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, The University of Chicago, Chicago, IL 60637, USA. hszz@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051618" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Autoantigens/immunology ; Cytokines/metabolism ; Fibroblasts/immunology/metabolism/*physiology ; Gelatinases/*metabolism ; Immune Tolerance ; Lymphocytes, Tumor-Infiltrating/*immunology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/*immunology/metabolism/pathology ; Serine Endopeptidases/*metabolism ; Stromal Cells/*immunology/metabolism ; T-Lymphocytes/*immunology/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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    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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    Body's hardworking microbes get some overdue respect (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1619. doi: 10.1126/science.330.6011.1619.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Physiological Phenomena ; Digestive System/microbiology ; Genes, Bacterial ; Genome, Bacterial ; Humans ; Immune System/physiology ; Metagenome/*physiology ; Metagenomics ; Mice ; Sequence Analysis, DNA ; *Virus Physiological Phenomena
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Shining a light on the genome's 'dark matter' (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1614. doi: 10.1126/science.330.6011.1614.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Intergenic/*genetics ; *Gene Expression Regulation ; *Genome ; *Genome, Human ; Humans ; Mice ; RNA Interference ; RNA, Untranslated/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: Presynaptic nerve terminals release neurotransmitters repeatedly, often at high frequency, and in relative isolation from neuronal cell bodies. Repeated release requires cycles of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-complex assembly and disassembly, with continuous generation of reactive SNARE-protein intermediates. Although many forms of neurodegeneration initiate presynaptically, only few pathogenic mechanisms are known, and the functions of presynaptic proteins linked to neurodegeneration, such as alpha-synuclein, remain unclear. Here, we show that maintenance of continuous presynaptic SNARE-complex assembly required a nonclassical chaperone activity mediated by synucleins. Specifically, alpha-synuclein directly bound to the SNARE-protein synaptobrevin-2/vesicle-associated membrane protein 2 (VAMP2) and promoted SNARE-complex assembly. Moreover, triple-knockout mice lacking synucleins developed age-dependent neurological impairments, exhibited decreased SNARE-complex assembly, and died prematurely. Thus, synucleins may function to sustain normal SNARE-complex assembly in a presynaptic terminal during aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235365/" 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/PMC3235365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burre, Jacqueline -- Sharma, Manu -- Tsetsenis, Theodoros -- Buchman, Vladimir -- Etherton, Mark R -- Sudhof, Thomas C -- 075615/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1663-7. doi: 10.1126/science.1195227. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304-5543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798282" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Cells, Cultured ; HSP40 Heat-Shock Proteins/metabolism ; Humans ; Membrane Fusion ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Nerve Degeneration/*metabolism ; Neurons/*metabolism ; Presynaptic Terminals/*metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; SNARE Proteins/*metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; alpha-Synuclein/chemistry/genetics/*metabolism
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    Parasympathetic innervation maintains epithelial progenitor cells during salivary organogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: The maintenance of a progenitor cell population as a reservoir of undifferentiated cells is required for organ development and regeneration. However, the mechanisms by which epithelial progenitor cells are maintained during organogenesis are poorly understood. We report that removal of the parasympathetic ganglion in mouse explant organ culture decreased the number and morphogenesis of keratin 5-positive epithelial progenitor cells. These effects were rescued with an acetylcholine analog. We demonstrate that acetylcholine signaling, via the muscarinic M1 receptor and epidermal growth factor receptor, increased epithelial morphogenesis and proliferation of the keratin 5-positive progenitor cells. Parasympathetic innervation maintained the epithelial progenitor cell population in an undifferentiated state, which was required for organogenesis. This mechanism for epithelial progenitor cell maintenance may be targeted for organ repair or regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376907/" 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/PMC3376907/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knox, S M -- Lombaert, I M A -- Reed, X -- Vitale-Cross, L -- Gutkind, J S -- Hoffman, M P -- Z99 DE999999/Intramural NIH HHS/ -- ZIA DE000707-08/Intramural NIH HHS/ -- ZIA DE000722-04/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1645-7. doi: 10.1126/science.1192046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Matrix and Morphogenesis Unit, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, NIH, 30 Convent Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929848" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Carbachol/metabolism/pharmacology ; Cell Differentiation ; Epithelial Cells/cytology/*physiology ; Epithelium/embryology/innervation ; Ganglia, Parasympathetic/cytology/embryology/*physiology ; Heparin-binding EGF-like Growth Factor ; Intercellular Signaling Peptides and Proteins/metabolism/pharmacology ; Keratin-5/analysis/genetics ; Male ; Mice ; Morphogenesis/drug effects ; Neurons/cytology/*physiology ; Organ Culture Techniques ; *Organogenesis ; Prostate/cytology/embryology/innervation ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, Muscarinic M1/metabolism ; Regeneration ; Signal Transduction ; Stem Cells/cytology/*physiology ; Submandibular Gland/cytology/*embryology/*innervation
    Print ISSN: 0036-8075
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    Immunology. CAR'ing for the skin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, Andrey S -- Huang, Yina -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1154-5. doi: 10.1126/science.1195337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA. shaw@pathology.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules/chemistry/*metabolism ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Crystallization ; Epidermis/*immunology/metabolism/ultrastructure ; Hydrogen Bonding ; Ligands ; Lymphocyte Activation ; Mice ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Receptors, Antigen, T-Cell, gamma-delta/*immunology/metabolism ; Receptors, Virus/chemistry/*metabolism ; Signal Transduction ; T-Lymphocyte Subsets/*immunology/*metabolism ; Tight Junctions/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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    Essential role of the histone methyltransferase G9a in cocaine-induced plasticity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-09
    Description: Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region, which was regulated by the cocaine-induced transcription factor DeltaFosB. Using conditional mutagenesis and viral-mediated gene transfer, we found that G9a down-regulation increased the dendritic spine plasticity of nucleus accumbens neurons and enhanced the preference for cocaine, thereby establishing a crucial role for histone methylation in the long-term actions of cocaine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maze, Ian -- Covington, Herbert E 3rd -- Dietz, David M -- LaPlant, Quincey -- Renthal, William -- Russo, Scott J -- Mechanic, Max -- Mouzon, Ezekiell -- Neve, Rachael L -- Haggarty, Stephen J -- Ren, Yanhua -- Sampath, Srihari C -- Hurd, Yasmin L -- Greengard, Paul -- Tarakhovsky, Alexander -- Schaefer, Anne -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-120001/DA/NIDA NIH HHS/ -- P01 DA008227-129001/DA/NIDA NIH HHS/ -- P01 DA008227-13/DA/NIDA NIH HHS/ -- P01 DA008227-14/DA/NIDA NIH HHS/ -- P01 DA008227-15/DA/NIDA NIH HHS/ -- P01 DA008227-16/DA/NIDA NIH HHS/ -- P01 DA008227-170003/DA/NIDA NIH HHS/ -- P01 DA008227-180003/DA/NIDA NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P01 DA010044-15/DA/NIDA NIH HHS/ -- P01 DA010044-150005/DA/NIDA NIH HHS/ -- P01 DA010044-159002/DA/NIDA NIH HHS/ -- P01 DA08227/DA/NIDA NIH HHS/ -- P0110044/PHS HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-02/DA/NIDA NIH HHS/ -- R01 DA007359-17/DA/NIDA NIH HHS/ -- R01 DA007359-18/DA/NIDA NIH HHS/ -- R01 DA007359-19/DA/NIDA NIH HHS/ -- R01 DA007359-20/DA/NIDA NIH HHS/ -- R01 DA007359-21/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA07359/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):213-6. doi: 10.1126/science.1179438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
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    Induction of broadly neutralizing H1N1 influenza antibodies by vaccination (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: The rapid dissemination of the 2009 pandemic influenza virus underscores the need for universal influenza vaccines that elicit protective immunity to diverse viral strains. Here, we show that vaccination with plasmid DNA encoding H1N1 influenza hemagglutinin (HA) and boosting with seasonal vaccine or replication-defective adenovirus 5 vector encoding HA stimulated the production of broadly neutralizing influenza antibodies. This prime/boost combination increased the neutralization of diverse H1N1 strains dating from 1934 to 2007 as compared to either component alone and conferred protection against divergent H1N1 viruses in mice and ferrets. These antibodies were directed to the conserved stem region of HA and were also elicited in nonhuman primates. Cross-neutralization of H1N1 subtypes elicited by this approach provides a basis for the development of a universal influenza vaccine for humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, Chih-Jen -- Boyington, Jeffrey C -- McTamney, Patrick M -- Kong, Wing-Pui -- Pearce, Melissa B -- Xu, Ling -- Andersen, Hanne -- Rao, Srinivas -- Tumpey, Terrence M -- Yang, Zhi-Yong -- Nabel, Gary J -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1060-4. doi: 10.1126/science.1192517. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD 20892-3005, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/biosynthesis/*immunology ; Antibodies, Viral/biosynthesis/*immunology ; *Cross Protection ; Female ; Ferrets ; Genetic Vectors ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/*immunology ; Humans ; Immunization, Secondary ; Influenza A Virus, H1N1 Subtype/*immunology ; Influenza A Virus, H2N2 Subtype/immunology ; Influenza A Virus, H3N2 Subtype/immunology ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza Vaccines/*administration & dosage/*immunology ; Influenza, Human/immunology/prevention & control ; Macaca mulatta ; Male ; Mice ; Mice, Inbred BALB C ; Mutant Proteins/immunology ; Orthomyxoviridae Infections/immunology/prevention & control ; Plasmids ; Vaccination ; Vaccines, DNA/administration & dosage/immunology
    Print ISSN: 0036-8075
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    PTIP promotes chromatin changes critical for immunoglobulin class switch recombination (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here, we showed that activated B cells deficient in the PTIP component of the MLL3 (mixed-lineage leukemia 3)-MLL4 complex display impaired trimethylation of histone 3 at lysine 4 (H3K4me3) and transcription initiation of downstream switch regions at the immunoglobulin heavy-chain (Igh) locus, leading to defective immunoglobulin class switching. We also showed that PTIP accumulation at DSBs contributes to class switch recombination (CSR) and genome stability independently of Igh switch transcription. These results demonstrate that PTIP promotes specific chromatin changes that control the accessibility of the Igh locus to CSR and suggest a nonredundant role for the MLL3-MLL4 complex in altering antibody effector function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008398/" 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/PMC3008398/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, Jeremy A -- Santos, Margarida Almeida -- Wang, Zhibin -- Zang, Chongzhi -- Schwab, Kristopher R -- Jankovic, Mila -- Filsuf, Darius -- Chen, Hua-Tang -- Gazumyan, Anna -- Yamane, Arito -- Cho, Young-Wook -- Sun, Hong-Wei -- Ge, Kai -- Peng, Weiqun -- Nussenzweig, Michel C -- Casellas, Rafael -- Dressler, Gregory R -- Zhao, Keji -- Nussenzweig, Andre -- Z01 AR041149-03/Intramural NIH HHS/ -- Z01 AR041149-04/Intramural NIH HHS/ -- Z01 DK047055-01/Intramural NIH HHS/ -- Z01 DK047055-02/Intramural NIH HHS/ -- Z01 DK075003-04/Intramural NIH HHS/ -- Z01 DK075003-05/Intramural NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- ZIA AR041149-05/Intramural NIH HHS/ -- ZIA DK075017-03/Intramural NIH HHS/ -- ZIADK047055-03/DK/NIDDK NIH HHS/ -- ZIADK075003-06/DK/NIDDK NIH HHS/ -- ZIADK075017-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):917-23. doi: 10.1126/science.1187942. Epub 2010 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity/genetics ; Carrier Proteins/genetics/*physiology ; Cytidine Deaminase/metabolism ; Dna ; Histones/metabolism ; Immunoglobulin Class Switching/genetics/*physiology ; Immunoglobulin Switch Region ; Methylation ; Mice ; Nuclear Proteins/genetics/*physiology ; Promoter Regions, Genetic ; Recombination, Genetic ; Transcriptional Activation
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    The Lmo2 oncogene initiates leukemia in mice by inducing thymocyte self-renewal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: The LMO2 oncogene causes a subset of human T cell acute lymphoblastic leukemias (T-ALL), including four cases that arose as adverse events in gene therapy trials. To investigate the cellular origin of LMO2-induced leukemia, we used cell fate mapping to study mice in which the Lmo2 gene was constitutively expressed in the thymus. Lmo2 induced self-renewal of committed T cells in the mice more than 8 months before the development of overt T-ALL. These self-renewing cells retained the capacity for T cell differentiation but expressed several genes typical of hematopoietic stem cells (HSCs), suggesting that Lmo2 might reactivate an HSC-specific transcriptional program. Forced expression of one such gene, Hhex, was sufficient to initiate self-renewal of thymocytes in vivo. Thus, Lmo2 promotes the self-renewal of preleukemic thymocytes, providing a mechanism by which committed T cells can then accumulate additional genetic mutations required for leukemic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCormack, Matthew P -- Young, Lauren F -- Vasudevan, Sumitha -- de Graaf, Carolyn A -- Codrington, Rosalind -- Rabbitts, Terence H -- Jane, Stephen M -- Curtis, David J -- G0600914/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):879-83. doi: 10.1126/science.1182378. Epub 2010 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rotary Bone Marrow Research Laboratories, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia. mccormack@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cell Differentiation ; Cell Transformation, Neoplastic/*genetics ; DNA-Binding Proteins/*genetics/metabolism ; Down-Regulation ; Gene Expression Profiling ; Gene Expression Regulation, Leukemic ; Homeodomain Proteins/genetics ; Humans ; LIM Domain Proteins ; Metalloproteins/*genetics/metabolism ; Mice ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Oncogenes ; Precursor Cells, T-Lymphoid/*physiology/transplantation ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism/pathology ; Preleukemia/genetics/metabolism/pathology ; Proto-Oncogene Proteins ; T-Lymphocyte Subsets ; T-Lymphocytes/*physiology/transplantation ; Thymus Gland/metabolism/pathology ; Transcription Factors/genetics ; Transcription, Genetic ; Up-Regulation
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    Genetic reactivation of cone photoreceptors restores visual responses in retinitis pigmentosa (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: Retinitis pigmentosa refers to a diverse group of hereditary diseases that lead to incurable blindness, affecting two million people worldwide. As a common pathology, rod photoreceptors die early, whereas light-insensitive, morphologically altered cone photoreceptors persist longer. It is unknown if these cones are accessible for therapeutic intervention. Here, we show that expression of archaebacterial halorhodopsin in light-insensitive cones can substitute for the native phototransduction cascade and restore light sensitivity in mouse models of retinitis pigmentosa. Resensitized photoreceptors activate all retinal cone pathways, drive sophisticated retinal circuit functions (including directional selectivity), activate cortical circuits, and mediate visually guided behaviors. Using human ex vivo retinas, we show that halorhodopsin can reactivate light-insensitive human photoreceptors. Finally, we identified blind patients with persisting, light-insensitive cones for potential halorhodopsin-based therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busskamp, Volker -- Duebel, Jens -- Balya, David -- Fradot, Mathias -- Viney, Tim James -- Siegert, Sandra -- Groner, Anna C -- Cabuy, Erik -- Forster, Valerie -- Seeliger, Mathias -- Biel, Martin -- Humphries, Peter -- Paques, Michel -- Mohand-Said, Saddek -- Trono, Didier -- Deisseroth, Karl -- Sahel, Jose A -- Picaud, Serge -- Roska, Botond -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):413-7. doi: 10.1126/science.1190897. Epub 2010 Jun 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Circuit Laboratories, Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dependovirus/genetics ; Disease Models, Animal ; Evoked Potentials, Visual ; *Genetic Therapy ; Genetic Vectors ; Halobacteriaceae/genetics ; Halorhodopsins/*genetics/*metabolism ; Humans ; Light ; Mice ; Mice, Knockout ; Promoter Regions, Genetic ; Retina/physiology ; Retinal Cone Photoreceptor Cells/*physiology ; Retinal Ganglion Cells/physiology ; Retinitis Pigmentosa/physiopathology/*therapy ; Tissue Culture Techniques ; Transfection ; Vision, Ocular ; Visual Pathways/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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    CKAMP44: a brain-specific protein attenuating short-term synaptic plasticity in the dentate gyrus (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: CKAMP44, identified here by a proteomic approach, is a brain-specific type I transmembrane protein that associates with AMPA receptors in synaptic spines. CKAMP44 expressed in Xenopus oocytes reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl-D-aspartate (NMDA) receptor-mediated currents. Mouse hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance, and overexpression of CKAMP44 led to stronger and faster AMPA receptor desensitization, slower recovery from desensitization, and a reduction in the paired-pulse ratio of AMPA currents. By contrast, dentate gyrus granule cells exhibited strong CKAMP44 expression, and CKAMP44 knockout increased the paired-pulse ratio of AMPA currents in lateral and medial perforant path-granule cell synapses. CKAMP44 thus modulates short-term plasticity at specific excitatory synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Engelhardt, Jakob -- Mack, Volker -- Sprengel, Rolf -- Kavenstock, Netta -- Li, Ka Wan -- Stern-Bach, Yael -- Smit, August B -- Seeburg, Peter H -- Monyer, Hannah -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1518-22. doi: 10.1126/science.1184178. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neurobiology, University of Heidelberg, 6910 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/metabolism ; Calcium Channels/metabolism ; Dendritic Spines/metabolism ; Dentate Gyrus/cytology/*metabolism ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Guanylate Kinase ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Miniature Postsynaptic Potentials ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neural Inhibition ; *Neuronal Plasticity ; Neurons/*metabolism ; Oocytes/metabolism ; Patch-Clamp Techniques ; Perforant Pathway ; Protein Interaction Domains and Motifs ; Protein Isoforms/genetics/metabolism ; Proteomics ; Pyramidal Cells/metabolism ; Receptors, AMPA/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Synapses/*physiology ; *Synaptic Transmission ; Xenopus laevis
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    Inhibition of NF-kappaB signaling by A20 through disruption of ubiquitin enzyme complexes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: A20 negatively regulates inflammation by inhibiting the nuclear factor kappaB (NF-kappaB) transcription factor in the tumor necrosis factor-receptor (TNFR) and Toll-like receptor (TLR) pathways. A20 contains deubiquitinase and E3 ligase domains and thus has been proposed to function as a ubiquitin-editing enzyme downstream of TNFR1 by inactivating ubiquitinated RIP1. However, it remains unclear how A20 terminates NF-kappaB signaling downstream of TLRs. We have shown that A20 inhibited the E3 ligase activities of TRAF6, TRAF2, and cIAP1 by antagonizing interactions with the E2 ubiquitin conjugating enzymes Ubc13 and UbcH5c. A20, together with the regulatory molecule TAX1BP1, interacted with Ubc13 and UbcH5c and triggered their ubiquitination and proteasome-dependent degradation. These findings suggest mechanism of A20 action in the inhibition of inflammatory signaling pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025292/" 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/PMC3025292/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shembade, Noula -- Ma, Averil -- Harhaj, Edward W -- R01 CA135362/CA/NCI NIH HHS/ -- R01 CA135362-04/CA/NCI NIH HHS/ -- R01 DK071939/DK/NIDDK NIH HHS/ -- R01 DK071939-07/DK/NIDDK NIH HHS/ -- R01 GM083143/GM/NIGMS NIH HHS/ -- R01 GM083143-03/GM/NIGMS NIH HHS/ -- R01CA135362/CA/NCI NIH HHS/ -- R01GM083143/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1135-9. doi: 10.1126/science.1182364.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Sylvester Comprehensive Cancer Center, The University of Miami, Miller School of Medicine, Miami, FL 33136, USA. nshembade@med.miami.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185725" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cells, Cultured ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Gene Products, tax/metabolism ; Inflammation/*metabolism ; Inhibitor of Apoptosis Proteins/antagonists & inhibitors/metabolism ; Interleukin-1/immunology/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Mice ; NF-kappa B/*metabolism ; Neoplasm Proteins/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 2/antagonists & inhibitors/metabolism ; TNF Receptor-Associated Factor 6/antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/immunology/metabolism ; Ubiquitin-Conjugating Enzymes/*metabolism ; Ubiquitin-Protein Ligases/*antagonists & inhibitors/metabolism ; Ubiquitinated Proteins/metabolism ; Ubiquitination ; Zinc Fingers
    Print ISSN: 0036-8075
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    FCHo proteins are nucleators of clathrin-mediated endocytosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: Clathrin-mediated endocytosis, the major pathway for ligand internalization into eukaryotic cells, is thought to be initiated by the clustering of clathrin and adaptors around receptors destined for internalization. However, here we report that the membrane-sculpting F-BAR domain-containing Fer/Cip4 homology domain-only proteins 1 and 2 (FCHo1/2) were required for plasma membrane clathrin-coated vesicle (CCV) budding and marked sites of CCV formation. Changes in FCHo1/2 expression levels correlated directly with numbers of CCV budding events, ligand endocytosis, and synaptic vesicle marker recycling. FCHo1/2 proteins bound specifically to the plasma membrane and recruited the scaffold proteins eps15 and intersectin, which in turn engaged the adaptor complex AP2. The FCHo F-BAR membrane-bending activity was required, leading to the proposal that FCHo1/2 sculpt the initial bud site and recruit the clathrin machinery for CCV formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883440/" 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/PMC2883440/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henne, William Mike -- Boucrot, Emmanuel -- Meinecke, Michael -- Evergren, Emma -- Vallis, Yvonne -- Mittal, Rohit -- McMahon, Harvey T -- MC_U105178795/Medical Research Council/United Kingdom -- U.1051.02.007(78795)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1281-4. doi: 10.1126/science.1188462. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology (MRC-LMB), Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448150" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 2/metabolism ; Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Calcium-Binding Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Clathrin/*metabolism ; Clathrin-Coated Vesicles/*metabolism ; *Endocytosis ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins ; Mice ; Models, Molecular ; Neurons/cytology/metabolism ; Phosphoproteins/metabolism ; Protein Multimerization ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/metabolism ; Synaptic Vesicles/metabolism
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    Immunology. Prime, boost, and broaden (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doms, Robert W -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1021-2. doi: 10.1126/science.1195116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA. doms@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798304" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/biosynthesis/*immunology ; Antibodies, Viral/biosynthesis/*immunology ; *Cross Protection ; Cross Reactions ; Ferrets ; Haplorhini ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology ; Humans ; Immunization Schedule ; Immunization, Secondary ; Influenza A Virus, H1N1 Subtype/*immunology ; Influenza A virus/*immunology ; Influenza Vaccines/*administration & dosage/*immunology ; Mice ; Vaccines, DNA/administration & dosage/immunology ; Vaccines, Inactivated/administration & dosage/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Intravascular danger signals guide neutrophils to sites of sterile inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, Braedon -- Pittman, Keir -- Menezes, Gustavo B -- Hirota, Simon A -- Slaba, Ingrid -- Waterhouse, Christopher C M -- Beck, Paul L -- Muruve, Daniel A -- Kubes, Paul -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):362-6. doi: 10.1126/science.1195491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947763" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion ; Chemokine CXCL2/metabolism ; Chemokines/metabolism ; Chemotaxis, Leukocyte ; Cues ; Endothelium, Vascular/physiology ; Inflammation/*immunology/metabolism/*pathology ; Kinetics ; Liver/blood supply/*immunology/metabolism/*pathology ; Liver Diseases/*immunology/metabolism/*pathology ; Macrophage-1 Antigen/physiology ; Mice ; Microscopy/methods ; Microscopy, Confocal ; Microvessels/physiology ; Necrosis ; *Neutrophil Infiltration ; Neutrophils/physiology ; Peptides/metabolism ; Receptors, Formyl Peptide/metabolism ; Receptors, Interleukin-8B/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7 ; Signal Transduction
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    Cell biology. Think vesicular chloride (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Andrew J -- Schwappach, Blanche -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1364-5. doi: 10.1126/science.1191529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Life Sciences, University of Manchester, Oxford Road, Manchester M13 9PT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chloride Channels/genetics/*metabolism ; Chlorides/*metabolism ; Endosomes/*metabolism ; Genetic Engineering ; Hydrogen-Ion Concentration ; Kidney Diseases/metabolism ; Lysosomes/*metabolism ; Membrane Potentials ; Mice ; *Protons
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    Suppression of antitumor immunity by stromal cells expressing fibroblast activation protein-alpha (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: The stromal microenvironment of tumors, which is a mixture of hematopoietic and mesenchymal cells, suppresses immune control of tumor growth. A stromal cell type that was first identified in human cancers expresses fibroblast activation protein-alpha (FAP). We created a transgenic mouse in which FAP-expressing cells can be ablated. Depletion of FAP-expressing cells, which made up only 2% of all tumor cells in established Lewis lung carcinomas, caused rapid hypoxic necrosis of both cancer and stromal cells in immunogenic tumors by a process involving interferon-gamma and tumor necrosis factor-alpha. Depleting FAP-expressing cells in a subcutaneous model of pancreatic ductal adenocarcinoma also permitted immunological control of growth. Therefore, FAP-expressing cells are a nonredundant, immune-suppressive component of the tumor microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraman, Matthew -- Bambrough, Paul J -- Arnold, James N -- Roberts, Edward W -- Magiera, Lukasz -- Jones, James O -- Gopinathan, Aarthi -- Tuveson, David A -- Fearon, Douglas T -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):827-30. doi: 10.1126/science.1195300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Immunology Unit, Department of Medicine, University of Cambridge, Medical Research Council Centre, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051638" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Cancer Vaccines/administration & dosage/immunology ; Carcinoma, Lewis Lung/*immunology/pathology/therapy ; Carcinoma, Pancreatic Ductal/*immunology/pathology ; Cell Hypoxia ; Cell Line, Tumor ; Cell Survival ; Gelatinases/*metabolism ; *Immune Tolerance ; Interferon-gamma/immunology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Transgenic ; Necrosis ; Neoplasm Transplantation ; Serine Endopeptidases/*metabolism ; Stromal Cells/*immunology/metabolism ; Tumor Microenvironment/*immunology ; Tumor Necrosis Factor-alpha/immunology/metabolism
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    Medicine. Refugee receptors switch sides (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorn, Gerald W 2nd -- R01 HL087871/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1586-7. doi: 10.1126/science.1188538.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. gdorn@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339055" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism/ultrastructure ; Cyclic AMP/*metabolism ; Heart Failure/*metabolism/pathology/physiopathology ; Humans ; Membrane Microdomains/metabolism ; Mice ; Myocardial Contraction ; Myocytes, Cardiac/*metabolism/ultrastructure ; Rats ; Receptors, Adrenergic, beta-1/*metabolism ; Receptors, Adrenergic, beta-2/*metabolism ; Sarcolemma/metabolism/ultrastructure ; Signal Transduction
    Print ISSN: 0036-8075
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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
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    An autophagy-enhancing drug promotes degradation of mutant alpha1-antitrypsin Z and reduces hepatic fibrosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: In the classical form of alpha1-antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver-derived secretory glycoprotein and renders it aggregation-prone. In addition to decreased serum concentrations of AT, the disorder is characterized by accumulation of the mutant alpha1-antitrypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain-of-toxic function mechanism. The proteasomal and autophagic pathways are known to mediate degradation of ATZ. Here we show that the autophagy-enhancing drug carbamazepine (CBZ) decreased the hepatic load of ATZ and hepatic fibrosis in a mouse model of AT deficiency-associated liver disease. These results provide a basis for testing CBZ, which has an extensive clinical safety profile, in patients with AT deficiency and also provide a proof of principle for therapeutic use of autophagy enhancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hidvegi, Tunda -- Ewing, Michael -- Hale, Pamela -- Dippold, Christine -- Beckett, Caroline -- Kemp, Carolyn -- Maurice, Nicholas -- Mukherjee, Amitava -- Goldbach, Christina -- Watkins, Simon -- Michalopoulos, George -- Perlmutter, David H -- DK076918/DK/NIDDK NIH HHS/ -- HL037784/HL/NHLBI NIH HHS/ -- R01 DK076918/DK/NIDDK NIH HHS/ -- R01 DK084512/DK/NIDDK NIH HHS/ -- RR022241/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):229-32. doi: 10.1126/science.1190354. Epub 2010 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*drug effects ; Carbamazepine/administration & dosage/*pharmacology/therapeutic use ; Cell Line ; Disease Models, Animal ; Endoplasmic Reticulum/metabolism ; HeLa Cells ; Humans ; Liver/drug effects/*metabolism/pathology ; Liver Cirrhosis/*drug therapy/etiology/metabolism/pathology ; Mice ; Mice, Transgenic ; Mutant Proteins/chemistry/metabolism ; Phagosomes/drug effects/ultrastructure ; Phenotype ; Proteasome Endopeptidase Complex/metabolism ; Protein Folding ; Solubility ; alpha 1-Antitrypsin/chemistry/genetics/*metabolism ; alpha 1-Antitrypsin Deficiency/complications/*metabolism/pathology
    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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    Neuroscience. Lynx for braking plasticity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3244692/" 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/PMC3244692/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Higley, Michael J -- Strittmatter, Stephen M -- R37 NS033020/NS/NINDS NIH HHS/ -- R37 NS033020-19/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1189-90. doi: 10.1126/science.1198983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cellular Neuroscience, Neurodegeneration and Repair Program, Department of Neurology, Yale University School of Medicine, New Haven, CT 06536, USA. michael.higley@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109660" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amblyopia/physiopathology/therapy ; Animals ; Chondroitin Sulfate Proteoglycans/physiology ; *Dominance, Ocular ; Membrane Glycoproteins/*genetics/*physiology ; Mice ; Mice, Knockout ; *Neuronal Plasticity ; Neuropeptides/*genetics/*physiology ; Nicotinic Antagonists ; Receptors, Immunologic/physiology ; Receptors, Nicotinic/metabolism ; Sensory Deprivation ; Signal Transduction ; *Vision, Ocular ; Visual Cortex/*physiology ; Visual Pathways/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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    mTORC1-mediated cell proliferation, but not cell growth, controlled by the 4E-BPs (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-29
    Description: The mammalian target of rapamycin complex 1 (mTORC1) integrates mitogen and nutrient signals to control cell proliferation and cell size. Hence, mTORC1 is implicated in a large number of human diseases--including diabetes, obesity, heart disease, and cancer--that are characterized by aberrant cell growth and proliferation. Although eukaryotic translation initiation factor 4E-binding proteins (4E-BPs) are critical mediators of mTORC1 function, their precise contribution to mTORC1 signaling and the mechanisms by which they mediate mTORC1 function have remained unclear. We inhibited the mTORC1 pathway in cells lacking 4E-BPs and analyzed the effects on cell size, cell proliferation, and cell cycle progression. Although the 4E-BPs had no effect on cell size, they inhibited cell proliferation by selectively inhibiting the translation of messenger RNAs that encode proliferation-promoting proteins and proteins involved in cell cycle progression. Thus, control of cell size and cell cycle progression appear to be independent in mammalian cells, whereas in lower eukaryotes, 4E-BPs influence both cell growth and proliferation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893390/" 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/PMC2893390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowling, Ryan J O -- Topisirovic, Ivan -- Alain, Tommy -- Bidinosti, Michael -- Fonseca, Bruno D -- Petroulakis, Emmanuel -- Wang, Xiaoshan -- Larsson, Ola -- Selvaraj, Anand -- Liu, Yi -- Kozma, Sara C -- Thomas, George -- Sonenberg, Nahum -- P50 NS057531/NS/NINDS NIH HHS/ -- P50 NS057531-01A2/NS/NINDS NIH HHS/ -- R01 DK078019/DK/NIDDK NIH HHS/ -- R01 DK73802/DK/NIDDK NIH HHS/ -- U01 CA84292-06/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1172-6. doi: 10.1126/science.1187532.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Montreal, Quebec H3A 1A3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508131" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Cell Cycle ; *Cell Enlargement ; Cell Line ; *Cell Proliferation ; Cell Size ; Cell Survival ; Eukaryotic Initiation Factors/genetics/*metabolism ; Humans ; Mice ; Mice, Knockout ; Multiprotein Complexes ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Protein Biosynthesis ; Proteins ; RNA, Messenger/genetics/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Transcription Factors/*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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    Essential regulation of CNS angiogenesis by the orphan G protein-coupled receptor GPR124 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-13
    Description: The orphan G protein-coupled receptor (GPCR) GPR124/tumor endothelial marker 5 is highly expressed in central nervous system (CNS) endothelium. Here, we show that complete null or endothelial-specific GPR124 deletion resulted in embryonic lethality from CNS-specific angiogenesis arrest in forebrain and neural tube. Conversely, GPR124 overexpression throughout all adult vascular beds produced CNS-specific hyperproliferative vascular malformations. In vivo, GPR124 functioned cell-autonomously in endothelium to regulate sprouting, migration, and developmental expression of the blood-brain barrier marker Glut1, whereas in vitro, GPR124 mediated Cdc42-dependent directional migration to forebrain-derived, vascular endothelial growth factor-independent cues. Our results demonstrate CNS-specific angiogenesis regulation by an endothelial receptor and illuminate functions of the poorly understood adhesion GPCR subfamily. Further, the functional tropism of GPR124 marks this receptor as a therapeutic target for CNS-related vascular pathologies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099479/" 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/PMC3099479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhnert, Frank -- Mancuso, Michael R -- Shamloo, Amir -- Wang, Hsiao-Ting -- Choksi, Vir -- Florek, Mareike -- Su, Hua -- Fruttiger, Marcus -- Young, William L -- Heilshorn, Sarah C -- Kuo, Calvin J -- 1DP2 OD006477/OD/NIH HHS/ -- 1R01HL074267/HL/NHLBI NIH HHS/ -- 1R01NS052830/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- 1R21 NS058600/NS/NINDS NIH HHS/ -- G0501711/Medical Research Council/United Kingdom -- GM07365/GM/NIGMS NIH HHS/ -- P01NS44155/NS/NINDS NIH HHS/ -- R01 CA095654/CA/NCI NIH HHS/ -- R01 CA095654-01/CA/NCI NIH HHS/ -- R01 HL074267/HL/NHLBI NIH HHS/ -- R01 HL074267-02/HL/NHLBI NIH HHS/ -- R01 NS052830/NS/NINDS NIH HHS/ -- R01 NS052830-01/NS/NINDS NIH HHS/ -- R01 NS064517/NS/NINDS NIH HHS/ -- R01 NS064517-02/NS/NINDS NIH HHS/ -- R01NS27713/NS/NINDS NIH HHS/ -- R21 NS070153/NS/NINDS NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):985-9. doi: 10.1126/science.1196554.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Hematology Division, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071672" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/abnormalities ; Blood-Brain Barrier/metabolism ; Cell Movement ; Embryonic Development ; Endothelial Cells/physiology ; Endothelium, Vascular/embryology/metabolism ; Gene Deletion ; Glucose Transporter Type 1/metabolism ; Mesencephalon/blood supply/embryology/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; *Neovascularization, Physiologic ; Neural Tube/*blood supply/embryology/metabolism ; Prosencephalon/*blood supply/embryology/metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Rhombencephalon/blood supply/embryology/metabolism ; Telencephalon/blood supply/embryology/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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    A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Leukotriene A(4) hydrolase (LTA(4)H) is a proinflammatory enzyme that generates the inflammatory mediator leukotriene B(4) (LTB(4)). LTA(4)H also possesses aminopeptidase activity with unknown substrate and physiological importance; we identified the neutrophil chemoattractant proline-glycine-proline (PGP) as this physiological substrate. PGP is a biomarker for chronic obstructive pulmonary disease (COPD) and is implicated in neutrophil persistence in the lung. In acute neutrophil-driven inflammation, PGP was degraded by LTA(4)H, which facilitated the resolution of inflammation. In contrast, cigarette smoke, a major risk factor for the development of COPD, selectively inhibited LTA(4)H aminopeptidase activity, which led to the accumulation of PGP and neutrophils. These studies imply that therapeutic strategies inhibiting LTA(4)H to prevent LTB(4) generation may not reduce neutrophil recruitment because of elevated levels of PGP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snelgrove, Robert J -- Jackson, Patricia L -- Hardison, Matthew T -- Noerager, Brett D -- Kinloch, Andrew -- Gaggar, Amit -- Shastry, Suresh -- Rowe, Steven M -- Shim, Yun M -- Hussell, Tracy -- Blalock, J Edwin -- 082727/Z/07/Z/Wellcome Trust/United Kingdom -- 1K23DK075788/DK/NIDDK NIH HHS/ -- 1R03DK084110-01/DK/NIDDK NIH HHS/ -- G0400795/Medical Research Council/United Kingdom -- G0802752/Medical Research Council/United Kingdom -- HL07783/HL/NHLBI NIH HHS/ -- HL087824/HL/NHLBI NIH HHS/ -- HL090999/HL/NHLBI NIH HHS/ -- HL102371-A1/HL/NHLBI NIH HHS/ -- K08HL091127/HL/NHLBI NIH HHS/ -- P171/03/C1/048/Medical Research Council/United Kingdom -- P30 DK079337/DK/NIDDK NIH HHS/ -- P30AR050948/AR/NIAMS NIH HHS/ -- P30CA13148/CA/NCI NIH HHS/ -- P50 AT00477/AT/NCCIH NIH HHS/ -- R01 HL077783/HL/NHLBI NIH HHS/ -- R01 HL077783-05/HL/NHLBI NIH HHS/ -- R01 HL087824/HL/NHLBI NIH HHS/ -- R01 HL087824-02/HL/NHLBI NIH HHS/ -- R01 HL090999/HL/NHLBI NIH HHS/ -- R01 HL090999-02S1/HL/NHLBI NIH HHS/ -- R01 HL090999-04/HL/NHLBI NIH HHS/ -- R01 HL102371/HL/NHLBI NIH HHS/ -- RR19231/RR/NCRR NIH HHS/ -- U54CA100949/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):90-4. doi: 10.1126/science.1190594. Epub 2010 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham Lung Health Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. rjs198@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813919" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Cells, Cultured ; Chemokines, CXC/metabolism ; Chemotaxis, Leukocyte ; Epoxide Hydrolases/antagonists & inhibitors/isolation & purification/*metabolism ; Female ; Humans ; Inflammation ; Leukotriene B4/metabolism ; Lung/*immunology/metabolism/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/enzymology/immunology/*physiology ; Oligopeptides/*metabolism ; Orthomyxoviridae Infections/immunology/metabolism/pathology ; Pneumococcal Infections/immunology/metabolism/pathology ; Pneumonia/*immunology/metabolism/pathology/therapy ; Proline/*analogs & derivatives/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology/metabolism/pathology ; *Smoke ; Tobacco
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    Generating a prion with bacterially expressed recombinant prion protein (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: The prion hypothesis posits that a misfolded form of prion protein (PrP) is responsible for the infectivity of prion disease. Using recombinant murine PrP purified from Escherichia coli, we created a recombinant prion with the attributes of the pathogenic PrP isoform: aggregated, protease-resistant, and self-perpetuating. After intracerebral injection of the recombinant prion, wild-type mice developed neurological signs in approximately 130 days and reached the terminal stage of disease in approximately 150 days. Characterization of diseased mice revealed classic neuropathology of prion disease, the presence of protease-resistant PrP, and the capability of serially transmitting the disease; these findings confirmed that the mice succumbed to prion disease. Thus, as postulated by the prion hypothesis, the infectivity in mammalian prion disease results from an altered conformation of PrP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893558/" 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/PMC2893558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fei -- Wang, Xinhe -- Yuan, Chong-Gang -- Ma, Jiyan -- R01 NS060729/NS/NINDS NIH HHS/ -- R01 NS060729-01A1/NS/NINDS NIH HHS/ -- R01NS060729/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1132-5. doi: 10.1126/science.1183748. Epub 2010 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/pathology ; Brain Chemistry ; Cell Line ; Endopeptidase K/metabolism ; Escherichia coli/genetics ; Female ; Glycosylation ; Liver/chemistry ; Mice ; Neurons/chemistry ; Phosphatidylglycerols/*chemistry ; PrPC Proteins/chemistry/pathogenicity ; PrPSc Proteins/analysis/*chemistry/*pathogenicity ; Prion Diseases/*etiology/pathology ; Prions/*chemistry/*pathogenicity ; Protein Folding ; RNA/*chemistry ; Recombinant Proteins/chemistry
    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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    Medicine. Clearing conformational disease (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sifers, Richard N -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):154-5. doi: 10.1126/science.1192681.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030, USA. rsifers@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/drug effects ; Carbamazepine/*pharmacology ; Humans ; Liver Cirrhosis/*drug therapy/etiology/metabolism ; Mice ; Mice, Transgenic ; Mutant Proteins/chemistry/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Conformation ; *Protein Folding ; alpha 1-Antitrypsin/*chemistry/genetics/*metabolism ; alpha 1-Antitrypsin Deficiency/complications/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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    Temperature as a universal resetting cue for mammalian circadian oscillators (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Environmental temperature cycles are a universal entraining cue for all circadian systems at the organismal level with the exception of homeothermic vertebrates. We report here that resistance to temperature entrainment is a property of the suprachiasmatic nucleus (SCN) network and is not a cell-autonomous property of mammalian clocks. This differential sensitivity to temperature allows the SCN to drive circadian rhythms in body temperature, which can then act as a universal cue for the entrainment of cell-autonomous oscillators throughout the body. Pharmacological experiments show that network interactions in the SCN are required for temperature resistance and that the heat shock pathway is integral to temperature resetting and temperature compensation in mammalian cells. These results suggest that the evolutionarily ancient temperature resetting response can be used in homeothermic animals to enhance internal circadian synchronization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625727/" 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/PMC3625727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buhr, Ethan D -- Yoo, Seung-Hee -- Takahashi, Joseph S -- P50 MH074924/MH/NIMH NIH HHS/ -- P50 MH074924-01/MH/NIMH NIH HHS/ -- P50 MH074924-02/MH/NIMH NIH HHS/ -- P50 MH074924-03/MH/NIMH NIH HHS/ -- P50 MH074924-04/MH/NIMH NIH HHS/ -- P50 MH074924-05/MH/NIMH NIH HHS/ -- T32 AG 20418/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):379-85. doi: 10.1126/science.1195262.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208-3520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947768" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/metabolism ; Benzhydryl Compounds/pharmacology ; Biological Clocks/*physiology ; *Body Temperature ; Body Temperature Regulation ; Calcium Channels, L-Type/physiology ; Cell Communication ; Circadian Rhythm/*physiology ; Cues ; DNA-Binding Proteins/metabolism ; Heat-Shock Response ; Lung/physiology ; Mice ; Pituitary Gland/physiology ; Pyrrolidinones/pharmacology ; Signal Transduction ; Suprachiasmatic Nucleus/cytology/*physiology ; Temperature ; Tissue Culture Techniques ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Vasoactive Intestinal Peptide/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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    Neuroscience. Questionable calcium (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirchhoff, Frank -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1212-3. doi: 10.1126/science.1187420.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Gottingen, Germany. frank.kirchhoff@uks.eu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Calcium/*metabolism ; Calcium Channels/metabolism ; *Calcium Signaling ; Endoplasmic Reticulum/metabolism ; Gene Deletion ; Hippocampus/cytology/physiology ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/genetics/metabolism ; *Long-Term Potentiation ; Mice ; Neurons/*physiology ; Neurotransmitter Agents/metabolism ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Synaptic Transmission ; TRPC Cation Channels/metabolism
    Print ISSN: 0036-8075
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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
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    Signaling kinase AMPK activates stress-promoted transcription via histone H2B phosphorylation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: The mammalian adenosine monophosphate-activated protein kinase (AMPK) is a serine-threonine kinase protein complex that is a central regulator of cellular energy homeostasis. However, the mechanisms by which AMPK mediates cellular responses to metabolic stress remain unclear. We found that AMPK activates transcription through direct association with chromatin and phosphorylation of histone H2B at serine 36. AMPK recruitment and H2B Ser36 phosphorylation colocalized within genes activated by AMPK-dependent pathways, both in promoters and in transcribed regions. Ectopic expression of H2B in which Ser36 was substituted by alanine reduced transcription and RNA polymerase II association to AMPK-dependent genes, and lowered cell survival in response to stress. Our results place AMPK-dependent H2B Ser36 phosphorylation in a direct transcriptional and chromatin regulatory pathway leading to cellular adaptation to stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922052/" 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/PMC3922052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bungard, David -- Fuerth, Benjamin J -- Zeng, Ping-Yao -- Faubert, Brandon -- Maas, Nancy L -- Viollet, Benoit -- Carling, David -- Thompson, Craig B -- Jones, Russell G -- Berger, Shelley L -- CA078831/CA/NCI NIH HHS/ -- CA09171/CA/NCI NIH HHS/ -- CA105463/CA/NCI NIH HHS/ -- MC_U120027537/Medical Research Council/United Kingdom -- MOP-93799/Canadian Institutes of Health Research/Canada -- P01 AG031862/AG/NIA NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- R01 CA078831/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1201-5. doi: 10.1126/science.1191241. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647423" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/*metabolism ; Adaptation, Physiological ; Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Enzyme Activation ; Gene Expression Regulation ; Histones/chemistry/*metabolism ; Humans ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Serine/metabolism ; Signal Transduction ; *Stress, Physiological ; *Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cortical plasticity induced by inhibitory neuron transplantation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: Critical periods are times of pronounced brain plasticity. During a critical period in the postnatal development of the visual cortex, the occlusion of one eye triggers a rapid reorganization of neuronal responses, a process known as ocular dominance plasticity. We have shown that the transplantation of inhibitory neurons induces ocular dominance plasticity after the critical period. Transplanted inhibitory neurons receive excitatory synapses, make inhibitory synapses onto host cortical neurons, and promote plasticity when they reach a cellular age equivalent to that of endogenous inhibitory neurons during the normal critical period. These findings suggest that ocular dominance plasticity is regulated by the execution of a maturational program intrinsic to inhibitory neurons. By inducing plasticity, inhibitory neuron transplantation may facilitate brain repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164148/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Froemke, Robert C -- Alvarez-Buylla, Arturo -- Stryker, Michael P -- Gandhi, Sunil P -- EY016317/EY/NEI NIH HHS/ -- F32 EY016317/EY/NEI NIH HHS/ -- F32 EY016317-03/EY/NEI NIH HHS/ -- P50 MH077972/MH/NIMH NIH HHS/ -- P50 MH077972-05/MH/NIMH NIH HHS/ -- R01 NS048528/NS/NINDS NIH HHS/ -- R01 NS048528-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1145-8. doi: 10.1126/science.1183962.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; *Dominance, Ocular ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; *Neuronal Plasticity ; Neurons/*transplantation ; Prosencephalon/cytology/embryology ; Sensory Deprivation ; Synapses/physiology ; Visual Cortex/growth & development/*physiology
    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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    Immunology. Double TIP-ping (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Harinder -- Demarco, Ignacio A -- New York, N.Y. -- Science. 2010 Aug 20;329(5994):914-5. doi: 10.1126/science.1194316.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Discovery Immunology, Genentech, San Francisco, CA 94080, USA. singh.harinder@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724627" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Antibody Specificity/*genetics ; B-Lymphocytes/*immunology ; Carrier Proteins/genetics/*physiology ; Cells, Cultured ; Chromatin/metabolism ; Cytidine Deaminase/*metabolism ; Dna ; DNA Breaks, Double-Stranded ; DNA Modification Methylases/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histones/metabolism ; Immunoglobulin Class Switching/genetics/*physiology ; Immunoglobulin Switch Region ; Lymphocyte Activation ; Methylation ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*physiology ; Promoter Regions, Genetic ; Recombination, Genetic ; Transcriptional Activation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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)
    Details
    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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    Circadian rhythms. Temperatures to communicate by (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edery, Isaac -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):329-30. doi: 10.1126/science.1197747.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biochemistry, Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ 08854, USA. edery@cabm.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; *Body Temperature ; Body Temperature Regulation ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/metabolism ; Gene Expression ; Heat-Shock Proteins/metabolism ; Heat-Shock Response ; Homeostasis ; Mice ; Suprachiasmatic Nucleus/*physiology ; Temperature ; Transcription Factors/metabolism
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    Defective cross-presentation of viral antigens in GILT-free mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: Gamma-interferon-inducible lysosomal thiolreductase (GILT) promotes major histocompatibility complex (MHC) class II-restricted presentation of exogenous antigens containing disulfide bonds. Here, we show that GILT also facilitates MHC class I-restricted recognition of such antigens by CD8+ T cells, or cross-presentation. GILT is essential for cross-presentation of a CD8+ T cell epitope of glycoprotein B (gB) from herpes simplex virus 1 (HSV-1) but not for its presentation by infected cells. Initiation of the gB-specific CD8+ T cell response during HSV-1 infection, or cross-priming, is highly GILT-dependent, as is initiation of the response to the envelope glycoproteins of influenza A virus. Efficient cross-presentation of disulfide-rich antigens requires a complex pathway involving GILT-mediated reduction, unfolding, and partial proteolysis, followed by translocation into the cytosol for proteasomal processing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925227/" 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/PMC2925227/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Reshma -- Cresswell, Peter -- R37 AI023081/AI/NIAID NIH HHS/ -- R37 AI023081-26/AI/NIAID NIH HHS/ -- R37AI23081/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1394-8. doi: 10.1126/science.1189176.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, 300 Cedar Street, Post Office Box 208011, New Haven, CT 06250-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538950" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/metabolism ; Animals ; Antigen Presentation ; Antigens, Viral/*immunology ; CD8-Positive T-Lymphocytes/immunology ; *Cross-Priming ; Cytosol/metabolism ; Dendritic Cells/immunology ; Epitopes, T-Lymphocyte/immunology ; H-2 Antigens/immunology ; HeLa Cells ; Herpes Simplex/*immunology/metabolism ; Herpesvirus 1, Human/*immunology ; Humans ; Influenza A virus/immunology ; Mice ; Orthomyxoviridae Infections/immunology ; Oxidoreductases/genetics/*metabolism ; Proteasome Endopeptidase Complex/metabolism ; Viral Envelope Proteins/*immunology/*metabolism
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    Immunology. A guardian of T cell fate (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Santo, James P -- R01 AR060723/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):44-5. doi: 10.1126/science.1191664.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Innate Immunity Unit, Institut Pasteur, Paris F-75724, France. james.di-santo@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cells, Cultured ; Cytokines/metabolism ; Gene Deletion ; Gene Expression Regulation ; Interleukin-7/physiology ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Mice ; Models, Biological ; Precursor Cells, T-Lymphoid/cytology/physiology ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/cytology/immunology/*physiology ; Tumor Suppressor Proteins/*genetics/*metabolism
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    Reconstituting organ-level lung functions on a chip (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: Here, we describe a biomimetic microsystem that reconstitutes the critical functional alveolar-capillary interface of the human lung. This bioinspired microdevice reproduces complex integrated organ-level responses to bacteria and inflammatory cytokines introduced into the alveolar space. In nanotoxicology studies, this lung mimic revealed that cyclic mechanical strain accentuates toxic and inflammatory responses of the lung to silica nanoparticles. Mechanical strain also enhances epithelial and endothelial uptake of nanoparticulates and stimulates their transport into the underlying microvascular channel. Similar effects of physiological breathing on nanoparticle absorption are observed in whole mouse lung. Mechanically active "organ-on-a-chip" microdevices that reconstitute tissue-tissue interfaces critical to organ function may therefore expand the capabilities of cell culture models and provide low-cost alternatives to animal and clinical studies for drug screening and toxicology applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, Dongeun -- Matthews, Benjamin D -- Mammoto, Akiko -- Montoya-Zavala, Martin -- Hsin, Hong Yuan -- Ingber, Donald E -- R01-ES016665/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1662-8. doi: 10.1126/science.1188302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576885" target="_blank"〉PubMed〈/a〉
    Keywords: Air ; Animals ; *Biomimetic Materials ; Blood-Air Barrier ; Capillaries/*physiology ; Capillary Permeability ; Cells, Cultured ; Endothelial Cells/*physiology ; Escherichia coli/immunology ; Humans ; Immunity, Innate ; Inflammation ; Lung/blood supply/physiology ; Mice ; *Microfluidic Analytical Techniques ; Microtechnology ; Nanoparticles/toxicity ; Neutrophil Infiltration ; Oxidative Stress ; Pneumocytes/*physiology ; Pulmonary Alveoli/*blood supply/cytology/immunology/*physiology ; Respiration ; Silicon Dioxide/toxicity ; Stress, Mechanical
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    Immunology. IgA changes the rules of memory (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-26
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652650/" 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/PMC3652650/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerutti, Andrea -- P01 AI061093/AI/NIAID NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1646-7. doi: 10.1126/science.1192488.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Catalan Institute for Research and Advanced Studies, IMIM-Hospital del Mar, Barcelona Biomedical Research Park, 08003 Barcelona, Spain. acerutti@imim.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/biosynthesis/*immunology ; B-Lymphocytes/immunology ; Dendritic Cells/immunology ; Escherichia coli/growth & development/*immunology ; Germ-Free Life ; Half-Life ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Immunoglobulin A/biosynthesis/*immunology ; Immunoglobulin G/biosynthesis/immunology ; *Immunologic Memory ; Intestinal Mucosa/*immunology/*microbiology ; Mice ; T-Lymphocytes, Regulatory/immunology
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    Prion strain mutation determined by prion protein conformational compatibility and primary structure (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Prions are infectious proteins composed of the abnormal disease-causing isoform PrPSc, which induces conformational conversion of the host-encoded normal cellular prion protein PrPC to additional PrPSc. The mechanism underlying prion strain mutation in the absence of nucleic acids remains unresolved. Additionally, the frequency of strains causing chronic wasting disease (CWD), a burgeoning prion epidemic of cervids, is unknown. Using susceptible transgenic mice, we identified two prevalent CWD strains with divergent biological properties but composed of PrPSc with indistinguishable biochemical characteristics. Although CWD transmissions indicated stable, independent strain propagation by elk PrPC, strain coexistence in the brains of deer and transgenic mice demonstrated unstable strain propagation by deer PrPC. The primary structures of deer and elk prion proteins differ at residue 226, which, in concert with PrPSc conformational compatibility, determines prion strain mutation in these cervids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097672/" 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/PMC4097672/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angers, Rachel C -- Kang, Hae-Eun -- Napier, Dana -- Browning, Shawn -- Seward, Tanya -- Mathiason, Candace -- Balachandran, Aru -- McKenzie, Debbie -- Castilla, Joaquin -- Soto, Claudio -- Jewell, Jean -- Graham, Catherine -- Hoover, Edward A -- Telling, Glenn C -- 1P01AI077774-01/AI/NIAID NIH HHS/ -- 2R01 NS040334-04/NS/NINDS NIH HHS/ -- N01-AI-25491/AI/NIAID NIH HHS/ -- P01 AI077774/AI/NIAID NIH HHS/ -- R01 NS049173/NS/NINDS NIH HHS/ -- T32 AI49795/AI/NIAID NIH HHS/ -- T32 DA022738/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1154-8. doi: 10.1126/science.1187107. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky Medical Center, Lexington, KY 40536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466881" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/pathology ; Brain Chemistry ; *Deer ; Disease Susceptibility ; Mice ; Mice, Transgenic ; Mutation ; PrPC Proteins/*chemistry/genetics ; PrPSc Proteins/analysis/*chemistry/genetics/pathogenicity ; Protein Conformation ; Protein Folding ; Selection, Genetic ; Serial Passage ; Species Specificity ; *Wasting Disease, Chronic/pathology/transmission
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    Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-23
    Description: The intracerebral injection of beta-amyloid-containing brain extracts can induce cerebral beta-amyloidosis and associated pathologies in susceptible hosts. We found that intraperitoneal inoculation with beta-amyloid-rich extracts induced beta-amyloidosis in the brains of beta-amyloid precursor protein transgenic mice after prolonged incubation times.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233904/" 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/PMC3233904/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisele, Yvonne S -- Obermuller, Ulrike -- Heilbronner, Gotz -- Baumann, Frank -- Kaeser, Stephan A -- Wolburg, Hartwig -- Walker, Lary C -- Staufenbiel, Matthias -- Heikenwalder, Mathias -- Jucker, Mathias -- P51 RR000165/RR/NCRR NIH HHS/ -- P51 RR000165-51/RR/NCRR NIH HHS/ -- RR-00165/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):980-2. doi: 10.1126/science.1194516. Epub 2010 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tubingen, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966215" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amyloid beta-Peptides/administration & dosage/*chemistry/metabolism ; Animals ; Brain/blood supply/*pathology ; Brain Chemistry ; Cerebral Amyloid Angiopathy/metabolism/pathology ; Female ; Injections, Intraperitoneal ; Mice ; Mice, Transgenic ; Plaque, Amyloid/pathology ; Prions/chemistry/metabolism ; Protein Folding ; Time Factors
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  • 90
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    c-di-AMP secreted by intracellular Listeria monocytogenes activates a host type I interferon response (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-29
    Description: Intracellular bacterial pathogens, such as Listeria monocytogenes, are detected in the cytosol of host immune cells. Induction of this host response is often dependent on microbial secretion systems and, in L. monocytogenes, is dependent on multidrug efflux pumps (MDRs). Using L. monocytogenes mutants that overexpressed MDRs, we identified cyclic diadenosine monophosphate (c-di-AMP) as a secreted molecule able to trigger the cytosolic host response. Overexpression of the di-adenylate cyclase, dacA (lmo2120), resulted in elevated levels of the host response during infection. c-di-AMP thus represents a putative bacterial secondary signaling molecule that triggers a cytosolic pathway of innate immunity and is predicted to be present in a wide variety of bacteria and archea.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156580/" 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/PMC3156580/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodward, Joshua J -- Iavarone, Anthony T -- Portnoy, Daniel A -- P01 AI063302/AI/NIAID NIH HHS/ -- P01 AI063302-03/AI/NIAID NIH HHS/ -- T32 CA 009179/CA/NCI NIH HHS/ -- T32 CA009179/CA/NCI NIH HHS/ -- T32 CA009179-35/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1703-5. doi: 10.1126/science.1189801. Epub 2010 May 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/metabolism ; Cytosol/immunology/microbiology ; Dinucleoside Phosphates/*metabolism ; Female ; Genes, Bacterial ; *Immunity, Innate ; Interferon-beta/*metabolism ; Ligands ; Listeria monocytogenes/genetics/immunology/*metabolism ; Macrophages/*immunology/*microbiology ; Mass Spectrometry ; Membrane Transport Proteins/metabolism ; Mice ; Operon ; Phosphorus-Oxygen Lyases/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Fast vesicle fusion in living cells requires at least three SNARE complexes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-18
    Description: Exocytosis requires formation of SNARE [soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor] complexes between vesicle and target membranes. Recent assessments in reduced model systems have produced divergent estimates of the number of SNARE complexes needed for fusion. Here, we used a titration approach to answer this question in intact, cultured chromaffin cells. Simultaneous expression of wild-type SNAP-25 and a mutant unable to support exocytosis progressively altered fusion kinetics and fusion-pore opening, indicating that both proteins assemble into heteromeric fusion complexes. Expressing different wild-type:mutant ratios revealed a third-power relation for fast (synchronous) fusion and a near-linear relation for overall release. Thus, fast fusion typically observed in synapses and neurosecretory cells requires at least three functional SNARE complexes, whereas slower release might occur with fewer complexes. Heterogeneity in SNARE-complex number may explain heterogeneity in vesicular release probability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mohrmann, Ralf -- de Wit, Heidi -- Verhage, Matthijs -- Neher, Erwin -- Sorensen, Jakob B -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):502-5. doi: 10.1126/science.1193134. Epub 2010 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane Biophysics, Max-Planck Institute for Biophysical Chemistry, Gottingen, Germany. Ralf.Mohrmann@uks.eu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847232" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/physiology ; Chromaffin Cells/physiology ; Cytoplasmic Vesicles/physiology ; Exocytosis/*physiology ; Green Fluorescent Proteins/genetics ; Membrane Fusion/*physiology ; Mice ; Mutation ; SNARE Proteins/physiology ; Synaptosomal-Associated Protein 25/genetics/*physiology
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    Immunology. Salmonella susceptibility (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moir, Susan -- Fauci, Anthony S -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):439-40. doi: 10.1126/science.1189088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. smoir@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413482" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/immunology ; Animals ; Antibodies, Bacterial/blood/*immunology ; Antibodies, Blocking/blood/*immunology ; Bacteremia/immunology ; Bacterial Outer Membrane Proteins/immunology ; Disease Susceptibility ; HIV Infections/complications/*immunology ; Humans ; Lipopolysaccharides/blood/*immunology ; Mice ; Salmonella/*immunology ; Salmonella Infections/*immunology
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    Dnmt3a-dependent nonpromoter DNA methylation facilitates transcription of neurogenic genes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-24
    Description: DNA methylation at proximal promoters facilitates lineage restriction by silencing cell type-specific genes. However, euchromatic DNA methylation frequently occurs in regions outside promoters. The functions of such nonproximal promoter DNA methylation are unclear. Here we show that the de novo DNA methyltransferase Dnmt3a is expressed in postnatal neural stem cells (NSCs) and is required for neurogenesis. Genome-wide analysis of postnatal NSCs indicates that Dnmt3a occupies and methylates intergenic regions and gene bodies flanking proximal promoters of a large cohort of transcriptionally permissive genes, many of which encode regulators of neurogenesis. Surprisingly, Dnmt3a-dependent nonproximal promoter methylation promotes expression of these neurogenic genes by functionally antagonizing Polycomb repression. Thus, nonpromoter DNA methylation by Dnmt3a may be used for maintaining active chromatin states of genes critical for development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539760/" 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/PMC3539760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Hao -- Coskun, Volkan -- Tao, Jifang -- Xie, Wei -- Ge, Weihong -- Yoshikawa, Kazuaki -- Li, En -- Zhang, Yi -- Sun, Yi Eve -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):444-8. doi: 10.1126/science.1190485.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Medical Pharmacology, University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. haowu7@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Brain/cytology/growth & development/*metabolism ; Chromatin Immunoprecipitation ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; *DNA Methylation ; DNA, Intergenic ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genome ; Histones/genetics/metabolism ; Mice ; Mice, Knockout ; Nervous System/growth & development ; Neurogenesis/*genetics ; Neuroglia/cytology ; Neurons/*cytology/metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Stem Cells/*metabolism ; *Transcription, Genetic
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    Axon extension occurs independently of centrosomal microtubule nucleation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-09
    Description: Microtubules are polymeric protein structures and components of the cytoskeleton. Their dynamic polymerization is important for diverse cellular functions. The centrosome is the classical site of microtubule nucleation and is thought to be essential for axon growth and neuronal differentiation--processes that require microtubule assembly. We found that the centrosome loses its function as a microtubule organizing center during development of rodent hippocampal neurons. Axons still extended and regenerated through acentrosomal microtubule nucleation, and axons continued to grow after laser ablation of the centrosome in early neuronal development. Thus, decentralized microtubule assembly enables axon extension and regeneration, and, after axon initiation, acentrosomal microtubule nucleation arranges the cytoskeleton, which is the source of the sophisticated morphology of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stiess, Michael -- Maghelli, Nicola -- Kapitein, Lukas C -- Gomis-Ruth, Susana -- Wilsch-Brauninger, Michaela -- Hoogenraad, Casper C -- Tolic-Norrelykke, Iva M -- Bradke, Frank -- New York, N.Y. -- Science. 2010 Feb 5;327(5966):704-7. doi: 10.1126/science.1182179. Epub 2010 Jan 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Independent Junior Research Group Axonal Growth and Regeneration, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/metabolism ; Axons/*physiology/ultrastructure ; Axotomy ; Centrosome/*physiology/ultrastructure ; Hippocampus/*cytology ; Mice ; Microtubule-Associated Proteins/metabolism ; Microtubules/*metabolism/ultrastructure ; Nerve Regeneration ; Neurogenesis ; Neurons/*physiology/ultrastructure ; Rats ; Tubulin/metabolism
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    Siah regulation of Pard3A controls neuronal cell adhesion during germinal zone exit (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: The brain's circuitry is established by directed migration and synaptogenesis of neurons during development. Although neurons mature and migrate in specific patterns, little is known about how neurons exit their germinal zone niche. We found that cerebellar granule neuron germinal zone exit is regulated by proteasomal degradation of Pard3A by the Seven in Absentia homolog (Siah) E3 ubiquitin ligase. Pard3A gain of function and Siah loss of function induce precocious radial migration. Time-lapse imaging using a probe to measure neuronal cell contact reveals that Pard3A promotes adhesive interactions needed for germinal zone exit by recruiting the epithelial tight junction adhesion molecule C to the neuronal cell surface. Our findings define a Siah-Pard3A signaling pathway that controls adhesion-dependent exit of neuronal progenitors or immature neurons from a germinal zone niche.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065828/" 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/PMC3065828/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Famulski, Jakub K -- Trivedi, Niraj -- Howell, Danielle -- Yang, Yuan -- Tong, Yiai -- Gilbertson, Richard -- Solecki, David J -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-07/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-33/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1834-8. doi: 10.1126/science.1198480. Epub 2010 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; *Cell Movement ; Cell Polarity ; Cerebellum/*cytology/embryology/*metabolism ; Dogs ; Humans ; Immunoglobulins/chemistry/metabolism ; Mice ; Morphogenesis ; Neurons/cytology/*physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; RNA Interference ; Signal Transduction ; Stem Cells/physiology ; Transfection ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
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    Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-05
    Description: Staphylococcus aureus is a major human pathogen that is resistant to numerous antibiotics in clinical use. We found two nonribosomal peptide secondary metabolites--the aureusimines, made by S. aureus--that are not antibiotics, but function as regulators of virulence factor expression and are necessary for productive infections. In vivo mouse models of bacteremia showed that strains of S. aureus unable to produce aureusimines were attenuated and/or cleared from major organs, including the spleen, liver, and heart. Targeting aureusimine synthesis may offer novel leads for anti-infective drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wyatt, Morgan A -- Wang, Wenliang -- Roux, Christelle M -- Beasley, Federico C -- Heinrichs, David E -- Dunman, Paul M -- Magarvey, Nathan A -- MOP-38002/Canadian Institutes of Health Research/Canada -- RA107380/RA/ARRA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):294-6. doi: 10.1126/science.1188888. Epub 2010 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biomedical Sciences, M. G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522739" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteremia/microbiology ; Dipeptides/chemistry/isolation & purification ; Heart/microbiology ; Hemolysis ; Liver/microbiology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Peptide Biosynthesis, Nucleic Acid-Independent ; Peptide Synthases/chemistry/genetics/metabolism ; Pyrazines/chemistry/*metabolism ; Spleen/microbiology ; Staphylococcal Infections/*microbiology ; Staphylococcus aureus/genetics/isolation & ; purification/*metabolism/*pathogenicity ; Virulence Factors/*metabolism
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    Self-assembly of filopodia-like structures on supported lipid bilayers (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-11
    Description: Filopodia are finger-like protrusive structures, containing actin bundles. By incubating frog egg extracts with supported lipid bilayers containing phosphatidylinositol 4,5 bisphosphate, we have reconstituted the assembly of filopodia-like structures (FLSs). The actin assembles into parallel bundles, and known filopodial components localize to the tip and shaft. The filopodia tip complexes self-organize--they are not templated by preexisting membrane microdomains. The F-BAR domain protein toca-1 recruits N-WASP, followed by the Arp2/3 complex and actin. Elongation proteins, Diaphanous-related formin, VASP, and fascin are recruited subsequently. Although the Arp2/3 complex is required for FLS initiation, it is not essential for elongation, which involves formins. We propose that filopodia form via clustering of Arp2/3 complex activators, self-assembly of filopodial tip complexes on the membrane, and outgrowth of actin bundles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982780/" 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/PMC2982780/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Kwonmoo -- Gallop, Jennifer L -- Rambani, Komal -- Kirschner, Marc W -- GM26875/GM/NIGMS NIH HHS/ -- R01 GM026875/GM/NIGMS NIH HHS/ -- R01 GM026875-34/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1341-5. doi: 10.1126/science.1191710.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829485" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/ultrastructure ; Actin-Related Protein 2-3 Complex/metabolism ; Actins/*metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/metabolism ; Humans ; Kinetics ; *Lipid Bilayers ; Membrane Microdomains ; Mice ; Microfilament Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; NADPH Dehydrogenase/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphoproteins/metabolism ; Pseudopodia/*metabolism/*ultrastructure ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal/metabolism ; Xenopus ; Xenopus Proteins/metabolism
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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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in vivo evidence demonstrating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK. Bid, Bim, and Puma triple-knockout mice showed the same developmental defects that are associated with deficiency of Bax and Bak, including persistent interdigital webs and imperforate vaginas. Genetic deletion of Bid, Bim, and Puma prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes, despite the presence of other BH3-only molecules. Thus, many forms of apoptosis require direct activation of BAX and BAK at the mitochondria by a member of the BID, BIM, or PUMA family of proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163443/" 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/PMC3163443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, Decheng -- Tu, Ho-Chou -- Kim, Hyungjin -- Wang, Gary X -- Bean, Gregory R -- Takeuchi, Osamu -- Jeffers, John R -- Zambetti, Gerard P -- Hsieh, James J-D -- Cheng, Emily H-Y -- P30CA21765/CA/NCI NIH HHS/ -- R01 CA125562/CA/NCI NIH HHS/ -- R01 CA125562-02/CA/NCI NIH HHS/ -- R01 CA125562-03/CA/NCI NIH HHS/ -- R01 CA125562-04/CA/NCI NIH HHS/ -- R01CA125562/CA/NCI NIH HHS/ -- R01GM083159/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1390-3. doi: 10.1126/science.1190217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/deficiency/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics/*metabolism ; Caspases/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Cytochromes c/metabolism ; Intracellular Membranes/metabolism ; Membrane Proteins/deficiency/genetics/*metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Models, Biological ; Neurons/*physiology ; Permeability ; Protein Multimerization ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Stress, Physiological ; T-Lymphocytes/physiology ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism ; bcl-2 Homologous Antagonist-Killer Protein/chemistry/genetics/*metabolism ; bcl-2-Associated X Protein/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Neuroscience. China's brain mappers zoom in on neural connections (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minogue, Kristen -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):747. doi: 10.1126/science.330.6005.747.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051608" target="_blank"〉PubMed〈/a〉
    Keywords: Anatomy, Cross-Sectional ; Animals ; Brain/*cytology ; *Brain Mapping/instrumentation/methods ; China ; Mice ; Microtomy ; Neural Pathways/*cytology ; Neurons/*cytology/ultrastructure ; *Tomography/instrumentation/methods
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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