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  • Rats  (290)
  • Chemistry
  • American Association for the Advancement of Science (AAAS)  (293)
  • Cell Press
  • 2000-2004  (293)
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  • 1
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    bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Olig1 and Olig2 are closely related basic helix-loop-helix (bHLH) transcription factors that are expressed in myelinating oligodendrocytes and their progenitor cells in the developing central nervous system (CNS). Olig2 is necessary for the specification of oligodendrocytes, but the biological functions of Olig1 during oligodendrocyte lineage development are poorly understood. We show here that Olig1 function in mice is required not to develop the brain but to repair it. Specifically, we demonstrate a genetic requirement for Olig1 in repairing the types of lesions that occur in patients with multiple sclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnett, Heather A -- Fancy, Stephen P J -- Alberta, John A -- Zhao, Chao -- Plant, Sheila R -- Kaing, Sovann -- Raine, Cedric S -- Rowitch, David H -- Franklin, Robin J M -- Stiles, Charles D -- 689/Multiple Sclerosis Society/United Kingdom -- NS08952/NS/NINDS NIH HHS/ -- NS11920/NS/NINDS NIH HHS/ -- NS4051/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2111-5.〈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/15604411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Basic Helix-Loop-Helix Transcription Factors ; Brain/growth & development/*physiology ; Cell Nucleus/metabolism ; Cuprizone/pharmacology ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Demyelinating Diseases/*physiopathology ; Ethidium/pharmacology ; Humans ; Lysophosphatidylcholines/pharmacology ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/physiopathology ; Myelin Sheath/*physiology ; Nerve Tissue Proteins/genetics/*metabolism/physiology ; Oligodendroglia/*physiology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/growth & development/*physiology ; Stem Cells/physiology ; Transcription Factors/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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  • 2
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    Nutrient availability regulates SIRT1 through a forkhead-dependent pathway (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Nutrient availability regulates life-span in a wide range of organisms. We demonstrate that in mammalian cells, acute nutrient withdrawal simultaneously augments expression of the SIRT1 deacetylase and activates the Forkhead transcription factor Foxo3a. Knockdown of Foxo3a expression inhibited the starvation-induced increase in SIRT1 expression. Stimulation of SIRT1 transcription by Foxo3a was mediated through two p53 binding sites present in the SIRT1 promoter, and a nutrient-sensitive physical interaction was observed between Foxo3a and p53. SIRT1 expression was not induced in starved p53-deficient mice. Thus, in mammalian cells, p53, Foxo3a, and SIRT1, three proteins separately implicated in aging, constitute a nutrient-sensing pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemoto, Shino -- Fergusson, Maria M -- Finkel, Toren -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2105-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604409" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Binding Sites ; Culture Media ; Culture Media, Serum-Free ; DNA-Binding Proteins/*metabolism ; Forkhead Transcription Factors ; Gene Deletion ; Genes, p53 ; Glucose ; HeLa Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; PC12 Cells ; Promoter Regions, Genetic ; RNA, Small Interfering/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Serum ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; *Starvation ; Transcription Factors/*metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/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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  • 3
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    Obesity research. New data on appetite-suppressing peptide challenge critics (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, Trisha -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1453-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite/*drug effects ; Appetite Depressants/administration & dosage/*pharmacology ; Body Weight/drug effects ; Dose-Response Relationship, Drug ; Gastric Emptying/drug effects ; Humans ; Macaca mulatta ; Peptide Fragments ; Peptide YY/administration & dosage/metabolism/*pharmacology ; Rats
    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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    Society for Neuroscience meeting. Brain cells may pay the price for a bad night's sleep (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2004 Nov 12;306(5699):1126.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; *Cell Hypoxia ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats/administration & dosage ; Exercise ; Hippocampus/*cytology/physiology ; Humans ; *Learning ; Long-Term Potentiation ; Memory ; Neurons/*physiology ; Rats ; Sleep Apnea Syndromes/*physiopathology
    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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  • 5
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    Lysosomal glycosphingolipid recognition by NKT cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-13
    Description: NKT cells represent a distinct lineage of T cells that coexpress a conserved alphabeta T cell receptor (TCR) and natural killer (NK) receptors. Although the TCR of NKT cells is characteristically autoreactive to CD1d, a lipid-presenting molecule, endogenous ligands for these cells have not been identified. We show that a lysosomal glycosphingolipid of previously unknown function, isoglobotrihexosylceramide (iGb3), is recognized both by mouse and human NKT cells. Impaired generation of lysosomal iGb3 in mice lacking beta-hexosaminidase b results in severe NKT cell deficiency, suggesting that this lipid also mediates development of NKT cells in the mouse. We suggest that expression of iGb3 in peripheral tissues may be involved in controlling NKT cell responses to infections and malignancy and in autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Dapeng -- Mattner, Jochen -- Cantu, Carlos 3rd -- Schrantz, Nicolas -- Yin, Ning -- Gao, Ying -- Sagiv, Yuval -- Hudspeth, Kelly -- Wu, Yun-Ping -- Yamashita, Tadashi -- Teneberg, Susann -- Wang, Dacheng -- Proia, Richard L -- Levery, Steven B -- Savage, Paul B -- Teyton, Luc -- Bendelac, Albert -- AI053725/AI/NIAID NIH HHS/ -- AI50847/AI/NIAID NIH HHS/ -- P20RR16459/RR/NCRR NIH HHS/ -- R01 AI38339/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1786-9. Epub 2004 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, Department of Pathology, Chicago, IL 60637, USA. dzhou@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539565" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD1/immunology/metabolism ; Antigens, CD1d ; Autoimmunity ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Dendritic Cells/immunology ; Galactosyltransferases/genetics/metabolism ; Globosides/chemistry/*immunology/metabolism ; Humans ; Hybridomas ; Infection/immunology ; Killer Cells, Natural/*immunology ; Ligands ; Lymphocyte Activation ; Lymphocyte Count ; Lysosomes/*metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Plant Lectins/immunology ; Rats ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Saposins/metabolism ; T-Lymphocyte Subsets/*immunology ; beta-N-Acetylhexosaminidases/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    A link between mRNA turnover and RNA interference in Arabidopsis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: In RNA interference (RNAi), double-stranded RNA (dsRNA) triggers degradation of homologous messenger RNA. In many organisms, RNA-dependent RNA polymerase (RdRp) is required to initiate or amplify RNAi, but the substrate for dsRNA synthesis in vivo is not known. Here, we show that RdRp-dependent transgene silencing in Arabidopsis was caused by mutation of XRN4, which is a ribonuclease (RNase) implicated in mRNA turnover by means of decapping and 5'-3' exonucleolysis. When both XRN4 and the RdRp were mutated, the plants accumulated decapped transgene mRNA. We propose that mRNAs lacking a cap structure become exposed to RdRp to initiate or maintain RNAi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gazzani, S -- Lawrenson, T -- Woodward, C -- Headon, D -- Sablowski, R -- BBS/E/J/00000594/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1046-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528448" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/*genetics ; Arabidopsis Proteins/genetics ; Exoribonucleases/genetics ; Gene Silencing ; Homeodomain Proteins/genetics ; Mutation ; Plant Proteins/genetics ; Plants, Genetically Modified ; RNA Caps ; *RNA Interference ; RNA Replicase/metabolism ; RNA, Messenger/*metabolism ; RNA, Plant/*metabolism ; Rats ; Recombinant Fusion Proteins/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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  • 7
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    Tracking SNARE complex formation in live endocrine cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: Syntaxin, synaptosome-associated protein of 25 kD (SNAP25), and vesicle-associated membrane protein/synaptobrevin are collectively called SNAP receptor (SNARE) proteins, and they catalyze neuronal exocytosis by forming a "core complex." The steps in core complex formation are unknown. Here, we monitored SNARE complex formation in vivo with the use of a fluorescent version of SNAP25. In PC12 cells, we found evidence for a syntaxin-SNAP25 complex that formed with high affinity, required only the amino-terminal SNARE motif of SNAP25, tolerated a mutation that blocks formation of other syntaxin-SNAP25 complexes, and assembled reversibly when Ca2+ entered cells during depolarization. The complex may represent a precursor to the core complex formed during a Ca2+-dependent priming step of exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉An, Seong J -- Almers, Wolfhard -- MH60600/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1042-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute L-474, Oregon Health Sciences University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528447" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/cytology ; Animals ; Bacterial Proteins ; Cell Line ; Fluorescence Resonance Energy Transfer ; Green Fluorescent Proteins ; Humans ; Luminescent Proteins ; Membrane Proteins/genetics/physiology ; Nerve Tissue Proteins/genetics/physiology ; PC12 Cells ; Qa-SNARE Proteins ; Rats ; Recombinant Fusion Proteins ; SNARE Proteins ; Synaptosomal-Associated Protein 25 ; Vesicular Transport Proteins/*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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  • 8
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    Hemoxygenase-2 is an oxygen sensor for a calcium-sensitive potassium channel (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: Modulation of calcium-sensitive potassium (BK) channels by oxygen is important in several mammalian tissues, and in the carotid body it is crucial to respiratory control. However, the identity of the oxygen sensor remains unknown. We demonstrate that hemoxygenase-2 (HO-2) is part of the BK channel complex and enhances channel activity in normoxia. Knockdown of HO-2 expression reduced channel activity, and carbon monoxide, a product of HO-2 activity, rescued this loss of function. Inhibition of BK channels by hypoxia was dependent on HO-2 expression and was augmented by HO-2 stimulation. Furthermore, carotid body cells demonstrated HO-2-dependent hypoxic BK channel inhibition, which indicates that HO-2 is an oxygen sensor that controls channel activity during oxygen deprivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Sandile E J -- Wootton, Phillippa -- Mason, Helen S -- Bould, Jonathan -- Iles, David E -- Riccardi, Daniela -- Peers, Chris -- Kemp, Paul J -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2093-7. Epub 2004 Nov 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528406" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Monoxide/*metabolism ; Carotid Body/*cytology/*physiology ; Cell Hypoxia ; Cell Line ; Heme/metabolism ; Heme Oxygenase (Decyclizing)/genetics/*metabolism ; Humans ; Immunoprecipitation ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Potentials ; NADP/metabolism ; Oxygen/*physiology ; Patch-Clamp Techniques ; Potassium Channels, Calcium-Activated ; RNA Interference ; RNA, Small Interfering/pharmacology ; Rats ; Transfection
    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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  • 9
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    Protein kinase C overactivity impairs prefrontal cortical regulation of working memory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: The prefrontal cortex is a higher brain region that regulates thought, behavior, and emotion using representational knowledge, operations often referred to as working memory. We tested the influence of protein kinase C (PKC) intracellular signaling on prefrontal cortical cognitive function and showed that high levels of PKC activity in prefrontal cortex, as seen for example during stress exposure, markedly impair behavioral and electrophysiological measures of working memory. These data suggest that excessive PKC activation can disrupt prefrontal cortical regulation of behavior and thought, possibly contributing to signs of prefrontal cortical dysfunction such as distractibility, impaired judgment, impulsivity, and thought disorder.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, S G -- Yuan, P X -- Wang, M -- Vijayraghavan, S -- Bloom, A K -- Davis, D J -- Gobeske, K T -- Sweatt, J D -- Manji, H K -- Arnsten, A F T -- AG06036/AG/NIA NIH HHS/ -- P50 MH068789/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):882-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale Medical School, 333 Cedar Street, New Haven, CT 06520-8001, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514161" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Alkaloids ; Animals ; Benzophenanthridines ; Carbolines/pharmacology ; Electrophysiology ; Enzyme Activation ; Female ; Imidazoles/pharmacology ; Lithium Carbonate/pharmacology ; Macaca mulatta ; Male ; Memory/drug effects/*physiology ; Neurons/drug effects/physiology ; Phenanthridines/pharmacology ; Prefrontal Cortex/enzymology/*physiology ; Protein Kinase C/antagonists & inhibitors/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha-1/physiology ; Signal Transduction ; Stress, Physiological/physiopathology ; Tetradecanoylphorbol Acetate/pharmacology ; Valproic Acid/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Medicine. A wily recruiter in the battle against toxic beta amyloid aggregation (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):791-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514121" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Peptides/*chemistry/metabolism/toxicity ; Animals ; Cell Death/drug effects ; Cells, Cultured ; Congo Red/*analogs & derivatives/*chemical ; synthesis/chemistry/*metabolism/*pharmacology ; Ligands ; Neurons/cytology/*drug effects ; Piperidines/*chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Conformation ; Rats ; Tacrolimus Binding Proteins/*metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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