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  • Phosphorylation  (63)
  • Malaysia
  • OBIS
  • Oceanography
  • American Association for the Advancement of Science (AAAS)  (63)
  • UNESCO
  • 2020-2023
  • 2010-2014
  • 2000-2004  (63)
  • 1995-1999
  • 1975-1979
  • 2003  (63)
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  • American Association for the Advancement of Science (AAAS)  (63)
  • UNESCO
  • Kluwer  (1)
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  • 2020-2023
  • 2010-2014
  • 2000-2004  (63)
  • 1995-1999
  • 1975-1979
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  • 1
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    Insulin signaling in health and disease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: The signaling pathways used by insulin have been identified [M. White, Insulin Signaling Pathway, Sci. STKE (Connections Map, as seen November 2003), http://stke.sciencemag.org/cgi/cm/cmp_12069]. Now our challenge is to understand how the failure of these signals is associated with obesity and the progressive failure of pancreatic beta cells that leads to diabetes. Whether better management of chronic inflammation can improve insulin action is an important area of investigation. Drugs that stimulate IRS2 (insulin receptor substrate protein 2) synthesis or signaling might be a good starting point. This knowledge will lead to rational strategies that prevent or cure diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, Morris F -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1710-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Joslin Diabetes Center, Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA. morris.white@joslin.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Diabetes Mellitus/etiology/*metabolism ; Diabetes Mellitus, Type 1/etiology/metabolism ; Diabetes Mellitus, Type 2/etiology/metabolism ; Humans ; Inflammation ; Insulin/*metabolism ; Insulin Receptor Substrate Proteins ; *Insulin Resistance ; Intracellular Signaling Peptides and Proteins ; Islets of Langerhans/metabolism ; Mice ; Models, Biological ; Obesity/etiology/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Receptor, Insulin/genetics/metabolism ; *Signal Transduction ; Somatomedins/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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  • 2
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    Immunology. The paracaspase connection (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- Lenardo, Michael J -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1515-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645834" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Apoptosis ; B-Lymphocytes/*immunology/metabolism ; Caspases ; Cell Nucleus/metabolism ; Cytokines/metabolism ; Gene Expression Regulation ; I-kappa B Kinase ; Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/chemistry/genetics/*metabolism ; Mice ; NF-kappa B/*metabolism ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Translocation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Diverse psychotomimetics act through a common signaling pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Three distinct classes of drugs: dopaminergic agonists (such as D-amphetamine), serotonergic agonists (such as LSD), and glutamatergic antagonists (such as PCP) all induce psychotomimetic states in experimental animals that closely resemble schizophrenia symptoms in humans. Here we implicate a common signaling pathway in mediating these effects. In this pathway, dopamine- and an adenosine 3',5'-monophosphate (cAMP)-regulated phospho-protein of 32 kilodaltons (DARPP-32) is phosphorylated or dephosphorylated at three sites, in a pattern predicted to cause a synergistic inhibition of protein phosphatase-1 and concomitant regulation of its downstream effector proteins glycogen synthesis kinase-3 (GSK-3), cAMP response element-binding protein (CREB), and c-Fos. In mice with a genetic deletion of DARPP-32 or with point mutations in phosphorylation sites of DARPP-32, the effects of D-amphetamine, LSD, and PCP on two behavioral parameters-sensorimotor gating and repetitive movements-were strongly attenuated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Tzavara, Eleni T -- Carruthers, Robert -- Rachleff, Ilan -- Wattler, Sigrid -- Nehls, Michael -- McKinzie, David L -- Fienberg, Allen A -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1412-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631045" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology ; Animals ; Brain/drug effects/*metabolism ; Central Nervous System Agents/*pharmacology ; Corpus Striatum/drug effects/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dextroamphetamine/pharmacology ; Dopamine/metabolism ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Frontal Lobe/drug effects/metabolism ; Genes, fos ; Glycogen Synthase Kinase 3/metabolism ; Lysergic Acid Diethylamide/pharmacology ; Male ; Mice ; Mice, Knockout ; Motor Activity/drug effects ; Nerve Tissue Proteins/metabolism ; Phencyclidine/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein Phosphatase 1 ; RNA, Messenger/genetics/metabolism ; Receptors, Dopamine D1/genetics/metabolism ; Reflex, Startle/drug effects ; *Signal Transduction ; Synaptic Transmission
    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. CO gas joins brain signaling team (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1320-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Calcium/metabolism ; Calmodulin/metabolism ; Carbon Monoxide/*metabolism ; Ejaculation ; Enzyme Activation ; Heme Oxygenase (Decyclizing)/genetics/*metabolism ; Intestines/innervation/physiology ; Neurons/metabolism ; Neurotransmitter Agents/*metabolism ; Nitric Oxide/metabolism ; Phosphorylation ; *Signal Transduction ; *Synaptic Transmission
    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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    Neuroscience. SPARring with spines (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Guido -- Brose, Nils -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1341-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Neuroscience, Max Planck Institute for Experimental Medicine, D-37075 Gottingen, Germany. gmeyer@em.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Cycle ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Dendrites/*physiology/ultrastructure ; Down-Regulation ; GTPase-Activating Proteins/chemistry/*metabolism ; Hippocampus/cytology/metabolism ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/metabolism ; Neuronal Plasticity/*physiology ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Kinases/*metabolism ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Recombinant Proteins/metabolism ; Signal Transduction ; Synapses/*physiology ; Two-Hybrid System Techniques ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/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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    Retraction in amoeboid cell motility powered by cytoskeletal dynamics (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Cells crawl by coupling protrusion of their leading edge with retraction of their cell body. Protrusion is generated by the polymerization and bundling of filaments, but the mechanism of retraction is less clear. We have reconstituted retraction in vitro by adding Yersinia tyrosine phosphatase to the major sperm protein-based motility apparatus assembled from Ascaris sperm extracts. Retraction in vitro parallels that observed in vivo and is generated primarily by disassembly and rearrangement of the cytoskeleton. Therefore, cytoskeletal dynamics alone, unassisted by conventional motors, are able to generate both of these central components of amoeboid locomotion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miao, Long -- Vanderlinde, Orion -- Stewart, Murray -- Roberts, Thomas M -- R37GM29994/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1405-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science, Florida State University, Tallahassee, FL 32306, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631043" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Adenosine Triphosphate/metabolism/pharmacology ; Animals ; Ascaris suum/*cytology/physiology ; Biopolymers ; Cell Adhesion ; Cell Extracts ; Cell Movement/*physiology ; Cytoplasmic Vesicles/physiology ; Cytoskeleton/*physiology ; Helminth Proteins/chemistry/metabolism/*physiology ; Hydrogen-Ion Concentration ; Male ; Myosins/physiology ; Phosphorylation ; Protein Tyrosine Phosphatases/metabolism ; Pseudopodia/physiology ; Spermatozoa/physiology/ultrastructure ; Yersinia enterocolitica/enzymology
    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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    Control of nutrient-sensitive transcription programs by the unconventional prefoldin URI (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Prefoldins (PFDs) are members of a recently identified, small-molecular weight protein family able to assemble into molecular chaperone complexes. Here we describe an unusually large member of this family, termed URI, that forms complexes with other small-molecular weight PFDs and with RPB5, a shared subunit of all three RNA polymerases. Functional analysis of the yeast and human orthologs of URI revealed that both are targets of nutrient signaling and participate in gene expression controlled by the TOR kinase. Thus, URI is a component of a signaling pathway that coordinates nutrient availability with gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gstaiger, Matthias -- Luke, Brian -- Hess, Daniel -- Oakeley, Edward J -- Wirbelauer, Christiane -- Blondel, Marc -- Vigneron, Marc -- Peter, Matthias -- Krek, Wilhelm -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institut, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615539" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; DNA-Directed RNA Polymerases/metabolism ; GATA Transcription Factors ; *Gene Expression Regulation/drug effects ; Humans ; *Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Protein Subunits/metabolism ; RNA Interference ; Repressor Proteins/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; *Signal Transduction ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic/drug effects ; 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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  • 8
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    Immunology. Switching off TCR signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malissen, Bernard -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1162-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, INSERM-CNRS, Marseille Cedex 9, France. bernardm@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615524" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD2/metabolism ; Cell Membrane/immunology/*metabolism ; Computer Simulation ; Cytoskeletal Proteins ; Endocytosis ; Ligands ; Lipid Bilayers ; Lymphocyte Activation ; Major Histocompatibility Complex ; Mice ; Models, Immunological ; Peptides/immunology/metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-cbl ; Receptor Aggregation ; Receptor-CD3 Complex, Antigen, T-Cell/immunology/metabolism ; Receptors, Antigen, T-Cell/immunology/*metabolism ; *Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; *Ubiquitin-Protein Ligases ; ZAP-70 Protein-Tyrosine Kinase ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    Separase regulates INCENP-Aurora B anaphase spindle function through Cdc14 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-08
    Description: The inner centromere-like protein (INCENP) forms a complex with the evolutionarily conserved family of Aurora Bkinases. The INCENP-Aurora complex helps coordinate chromosome segregation, spindle behavior, and cytokinesis during mitosis. INCENP-Aurora associates with kinetochores in metaphase and with spindle microtubules in anaphase, yet the trigger for this abrupt transfer is unknown. Here we show that the conserved phosphatase Cdc14 regulated the yeast INCENP-Aurora complex, Sli15-Ipl1. Cdc14 dephosphorylated Sli15 and thereby directed the complex to spindles. Activation of Cdc14 by separase was sufficient for Sli15 dephosphorylation and relocalization. Cdc14 not only regulates mitotic exit but also modulates spindle midzone assembly through Sli15-Ipl1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pereira, Gislene -- Schiebel, Elmar -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2120-4. Epub 2003 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Paterson Institute for Cancer Research, Wilmslow Road, Manchester M20 4BX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605209" target="_blank"〉PubMed〈/a〉
    Keywords: *Anaphase ; Aurora Kinases ; Cell Cycle Proteins/*metabolism ; Cell Nucleolus/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Endopeptidases/*metabolism ; Intracellular Signaling Peptides and Proteins ; Kinetochores/metabolism ; Metaphase ; Microtubule-Associated Proteins/*metabolism ; Microtubules/metabolism ; Mitosis ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Protein Tyrosine Phosphatases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Saccharomyces cerevisiae/*cytology/metabolism ; Saccharomyces cerevisiae Proteins/*metabolism ; Separase ; Spindle Apparatus/*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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  • 10
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    Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, 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/14593183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*genetics ; Calcium/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; *Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Electrophoretic Mobility Shift Assay ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Methylation ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Phosphorylation ; Potassium Chloride/pharmacology ; Precipitin Tests ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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