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  • Mice  (61)
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  • American Association for the Advancement of Science (AAAS)  (61)
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  • 2010-2014  (61)
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  • 1
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    Dysregulated humoral immunity to nontyphoidal Salmonella in HIV-infected African adults (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-04-24
    Beschreibung: Nontyphoidal Salmonellae are a major cause of life-threatening bacteremia among HIV-infected individuals. Although cell-mediated immunity controls intracellular infection, antibodies protect against Salmonella bacteremia. We report that high-titer antibodies specific for Salmonella lipopolysaccharide (LPS) are associated with a lack of Salmonella-killing in HIV-infected African adults. Killing was restored by genetically shortening LPS from the target Salmonella or removing LPS-specific antibodies from serum. Complement-mediated killing of Salmonella by healthy serum is shown to be induced specifically by antibodies against outer membrane proteins. This killing is lost when excess antibody against Salmonella LPS is added. Thus, our study indicates that impaired immunity against nontyphoidal Salmonella bacteremia in HIV infection results from excess inhibitory antibodies against Salmonella LPS, whereas serum killing of Salmonella is induced by antibodies against outer membrane proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772309/" 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/PMC3772309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacLennan, Calman A -- Gilchrist, James J -- Gordon, Melita A -- Cunningham, Adam F -- Cobbold, Mark -- Goodall, Margaret -- Kingsley, Robert A -- van Oosterhout, Joep J G -- Msefula, Chisomo L -- Mandala, Wilson L -- Leyton, Denisse L -- Marshall, Jennifer L -- Gondwe, Esther N -- Bobat, Saeeda -- Lopez-Macias, Constantino -- Doffinger, Rainer -- Henderson, Ian R -- Zijlstra, Eduard E -- Dougan, Gordon -- Drayson, Mark T -- MacLennan, Ian C M -- Molyneux, Malcolm E -- 067321/Wellcome Trust/United Kingdom -- BB/F022778/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0701275/Medical Research Council/United Kingdom -- G108/574/Medical Research Council/United Kingdom -- G8402371/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):508-12. doi: 10.1126/science.1180346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Centre for Immune Regulation and Clinical Immunology Service, Institute of Biomedical Research, School of Immunity and Infection, University of Birmingham, Birmingham, UK. c.maclennan@bham.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413503" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): AIDS-Related Opportunistic Infections/immunology ; Adult ; Animals ; Antibodies, Bacterial/blood/*immunology ; Antibodies, Blocking/blood/*immunology ; Bacteremia/immunology ; Bacterial Outer Membrane Proteins/*immunology ; Complement Activation ; Disease Susceptibility ; HIV Infections/complications/*immunology ; Humans ; Immunoglobulin G/blood/immunology ; Lipopolysaccharides/blood/*immunology ; Malawi ; Mice ; Mutation ; O Antigens/*immunology ; Salmonella Infections/*immunology ; Salmonella typhimurium/genetics/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-05-22
    Beschreibung: Elevated leukocyte cell numbers (leukocytosis), and monocytes in particular, promote atherosclerosis; however, how they become increased is poorly understood. Mice deficient in the adenosine triphosphate-binding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages and suppress atherosclerosis in hypercholesterolemic mice, displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow. Transplantation of Abca1(-/-) Abcg1(-/-) bone marrow into apolipoprotein A-1 transgenic mice with elevated levels of high-density lipoprotein (HDL) suppressed the LSK population, reduced leukocytosis, reversed the myeloproliferative disorder, and accelerated atherosclerosis. The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoietic stem and multipotential progenitor cells and connect expansion of these populations with leukocytosis and accelerated atherosclerosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032591/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yvan-Charvet, Laurent -- Pagler, Tamara -- Gautier, Emmanuel L -- Avagyan, Serine -- Siry, Read L -- Han, Seongah -- Welch, Carrie L -- Wang, Nan -- Randolph, Gwendalyn J -- Snoeck, Hans W -- Tall, Alan R -- HL54591/HL/NHLBI NIH HHS/ -- R01 AG029626/AG/NIA NIH HHS/ -- R01 AI049653/AI/NIAID NIH HHS/ -- R01 AI049653-09/AI/NIAID NIH HHS/ -- R01 AI049653-10/AI/NIAID NIH HHS/ -- R01 AI061741/AI/NIAID NIH HHS/ -- R01 AI061741-03/AI/NIAID NIH HHS/ -- R01 AI061741-04/AI/NIAID NIH HHS/ -- R01A1061741/PHS HHS/ -- R01AG016327/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1689-93. doi: 10.1126/science.1189731. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY 10032, USA. ly2159@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488992" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Apolipoprotein A-I/genetics/metabolism ; Atherosclerosis/metabolism/*physiopathology/therapy ; Bone Marrow Transplantation ; Cell Proliferation ; Cells, Cultured ; Cholesterol/*metabolism ; Hematopoietic Stem Cells/*physiology ; Hypercholesterolemia/metabolism ; Leukocytosis/metabolism/*physiopathology/therapy ; Lipoproteins/genetics/*metabolism ; Lipoproteins, HDL/*metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Multipotent Stem Cells/physiology ; Myeloid Progenitor Cells/*physiology ; Myeloproliferative Disorders/metabolism/physiopathology/therapy ; Phenotype ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Receptors, Interleukin-3/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Altered histone acetylation is associated with age-dependent memory impairment in mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-05-08
    Beschreibung: As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peleg, Shahaf -- Sananbenesi, Farahnaz -- Zovoilis, Athanasios -- Burkhardt, Susanne -- Bahari-Javan, Sanaz -- Agis-Balboa, Roberto Carlos -- Cota, Perla -- Wittnam, Jessica Lee -- Gogol-Doering, Andreas -- Opitz, Lennart -- Salinas-Riester, Gabriella -- Dettenhofer, Markus -- Kang, Hui -- Farinelli, Laurent -- Chen, Wei -- Fischer, Andre -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):753-6. doi: 10.1126/science.1186088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Aging and Cognitive Diseases, European Neuroscience Institute, Grisebach Str. 5, D-37077 Goettingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448184" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Aging/*genetics ; Animals ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; Conditioning (Psychology) ; Epigenesis, Genetic ; Fear ; Gene Expression Profiling ; *Gene Expression Regulation ; Hippocampus/*metabolism ; Histone Deacetylase Inhibitors/metabolism/pharmacology ; Histones/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Lysine/metabolism ; Memory/drug effects ; Memory Disorders/*genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/genetics/metabolism ; Nuclear Proteins/genetics/metabolism ; Signal Transduction ; Transcription Initiation Site ; Transcription, Genetic ; Up-Regulation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Extending healthy life span--from yeast to humans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-04-17
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Male mice not alone in research (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-05-29
    Beschreibung: 〈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〉
    Schlagwort(e): *Animal Experimentation ; Animals ; Bias (Epidemiology) ; *Biomedical Research ; Female ; Male ; Mice ; *Models, Animal ; Sex Characteristics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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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
    Publikationsdatum: 2010-01-09
    Beschreibung: 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〉
    Schlagwort(e): Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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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
    Publikationsdatum: 2010-07-22
    Beschreibung: 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〉
    Schlagwort(e): 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
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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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
    Publikationsdatum: 2010-01-02
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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    Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-06-12
    Beschreibung: T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Burke, Shannon -- Wang, Juexuan -- Chen, Xiongfeng -- Ortiz, Mariaestela -- Lee, Song-Choon -- Lu, Dong -- Campos, Lia -- Goulding, David -- Ng, Bee Ling -- Dougan, Gordon -- Huntly, Brian -- Gottgens, Bertie -- Jenkins, Nancy A -- Copeland, Neal G -- Colucci, Francesco -- Liu, Pentao -- 076962/Wellcome Trust/United Kingdom -- 077186/Wellcome Trust/United Kingdom -- G0501150/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- G116/187/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):85-9. doi: 10.1126/science.1188063. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538915" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line, Tumor ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Cytotoxicity, Immunologic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, T-Cell Receptor beta ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Melanoma, Experimental/immunology/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Precursor Cells, T-Lymphoid/cytology/physiology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; Stromal Cells/cytology/physiology ; T-Lymphocytes/cytology/immunology/*physiology/transplantation ; Tamoxifen/analogs & derivatives/pharmacology ; Tumor Suppressor Proteins/*genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Calcium-permeable AMPA receptor dynamics mediate fear memory erasure (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-10-30
    Beschreibung: Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001394/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clem, Roger L -- Huganir, Richard L -- F32 MH087037-01/MH/NIMH NIH HHS/ -- R01 NS036715/NS/NINDS NIH HHS/ -- R01 NS036715-11/NS/NINDS NIH HHS/ -- R01NS036715/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1108-12. doi: 10.1126/science.1195298. Epub 2010 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030604" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amygdala/metabolism ; Animals ; Calcium/metabolism ; Conditioning (Psychology) ; *Extinction, Psychological ; Fear/*physiology ; Long-Term Synaptic Depression ; Male ; Memory/*physiology ; Mice ; Mice, Inbred C57BL ; Receptors, AMPA/*metabolism ; Receptors, Glutamate/metabolism ; Thalamus/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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