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  • Articles  (90)
  • Signal Transduction  (90)
  • 2000-2004  (90)
  • 2003  (90)
  • Chemistry and Pharmacology  (90)
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  • Articles  (90)
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  • 2000-2004  (90)
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  • 1
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    Neuroscience. ORs rule the roost in the olfactory system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewcock, Joseph W -- Reed, Randall R -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2078-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, 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/14684811" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alleles ; Animals ; Cell Nucleus/metabolism ; Chromosomes, Artificial, Yeast ; Feedback, Physiological ; *Gene Expression Regulation ; Genes, Reporter ; Mice ; Mice, Transgenic ; Multigene Family ; Odors ; Olfactory Receptor Neurons/*metabolism ; Promoter Regions, Genetic ; Pseudogenes ; Receptors, Odorant/*genetics/*metabolism ; Signal Transduction ; Transgenes
    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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    Redistribution of intracellular oxygen in hypoxia by nitric oxide: effect on HIF1alpha (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Cells exposed to low oxygen concentrations respond by initiating defense mechanisms, including the stabilization of hypoxia-inducible factor (HIF) 1alpha, a transcription factor that upregulates genes such as those involved in glycolysis and angiogenesis. Nitric oxide and other inhibitors of mitochondrial respiration prevent the stabilization of HIF1alpha during hypoxia. In studies of cultured cells, we show that this effect is a result of an increase in prolyl hydroxylase-dependent degradation of HIF1alpha. With the use of Renilla luciferase to detect intracellular oxygen concentrations, we also demonstrate that, upon inhibition of mitochondrial respiration in hypoxia, oxygen is redistributed toward nonrespiratory oxygen-dependent targets such as prolyl hydroxylases so that they do not register hypoxia. Thus, the signaling consequences of hypoxia may be profoundly modified by nitric oxide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagen, Thilo -- Taylor, Cormac T -- Lam, Francis -- Moncada, Salvador -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671307" target="_blank"〉PubMed〈/a〉
    Keywords: Antioxidants/pharmacology ; *Cell Hypoxia ; Cell Line ; *Cell Respiration/drug effects ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Leupeptins/*pharmacology ; Luciferases/metabolism ; Methacrylates ; Mitochondria/*metabolism ; Nitric Oxide/pharmacology/*physiology ; Nitric Oxide Donors/pharmacology ; Oxygen/*metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thiazoles/pharmacology ; Transcription Factors/*metabolism ; Transfection ; Triazenes/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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  • 3
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    Cell biology. Smurfing at the leading edge (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaffe, Aron B -- Hall, Alan -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1690-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, London WC1E 6BT, UK. a.jaffe@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*metabolism ; *Cell Movement ; *Cell Polarity ; GTPase-Activating Proteins/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Mice ; Protein Kinase C/metabolism ; Pseudopodia/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism ; cdc42 GTP-Binding Protein/metabolism ; rac GTP-Binding Proteins/metabolism ; rho GTP-Binding Proteins/*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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  • 4
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    Regulation of cell polarity and protrusion formation by targeting RhoA for degradation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: The Rho family of small guanosine triphosphatases regulates actin cytoskeleton dynamics that underlie cellular functions such as cell shape changes, migration, and polarity. We found that Smurf1, a HECT domain E3 ubiquitin ligase, regulated cell polarity and protrusive activity and was required to maintain the transformed morphology and motility of a tumor cell. Atypical protein kinase C zeta (PKCzeta), an effector of the Cdc42/Rac1-PAR6 polarity complex, recruited Smurf1 to cellular protrusions, where it controlled the local level of RhoA. Smurf1 thus links the polarity complex to degradation of RhoA in lamellipodia and filopodia to prevent RhoA signaling during dynamic membrane movements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong-Rui -- Zhang, Yue -- Ozdamar, Barish -- Ogunjimi, Abiodun A -- Alexandrova, Evguenia -- Thomsen, Gerald H -- Wrana, Jeffrey L -- HD32429/HD/NICHD NIH HHS/ -- R01 HD032429/HD/NICHD NIH HHS/ -- R01 HD032429-06/HD/NICHD NIH HHS/ -- R01 HD032429-07/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto M56 1x5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism/physiology ; *Cell Movement ; *Cell Polarity ; Cell Size ; Cell Transformation, Neoplastic ; Cytoskeleton/ultrastructure ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Intercellular Junctions/metabolism ; Mice ; NIH 3T3 Cells ; Protein Kinase C/metabolism ; Protein Structure, Tertiary ; Pseudopodia/*metabolism/ultrastructure ; RNA, Small Interfering ; Signal Transduction ; Transfection ; Ubiquitin-Protein Ligases/chemistry/genetics/*metabolism ; cdc42 GTP-Binding Protein/metabolism ; rhoA GTP-Binding Protein/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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  • 5
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    Neuroscience. Microglia: the enemy within? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kempermann, Gerd -- Neumann, Harald -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuronal Stem Cells Research Group, Max-Delbruck-Centrum fur Molekulare Medizin Berlin-Buch, 13125 Berlin, Germany. gerd.kempermann@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657479" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Brain-Derived Neurotrophic Factor/physiology ; Cell Differentiation ; Hippocampus/cytology/immunology/*physiology/radiation effects ; Immunity, Innate ; Inflammation/drug therapy/*physiopathology ; Inflammation Mediators/physiology ; Interleukin-6/*physiology ; Lipopolysaccharides/pharmacology ; Mice ; Microglia/*physiology ; Minocycline/pharmacology ; Neuronal Plasticity/drug effects ; Neurons/*physiology ; Rats ; Signal Transduction ; Stem Cells/physiology/radiation effects
    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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    Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: During apoptosis, phosphatidylserine, which is normally restricted to the inner leaflet of the plasma membrane, is exposed on the surface of apoptotic cells and has been suggested to act as an "eat-me" signal to trigger phagocytosis. It is unclear how phagocytes recognize phosphatidylserine. Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis. We report that psr-1, the Caenorhabditis elegans homolog of PSR, is important for cell corpse engulfment. In vitro PSR-1 binds preferentially phosphatidylserine or cells with exposed phosphatidylserine. In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular signaling molecules CED-2 (homologous to the human CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct interaction with CED-5 and CED-12. Our findings suggest that PSR-1 is likely an upstream receptor for the signaling pathway containing CED-2, CED-5, CED-10, and CED-12 proteins and plays an important role in recognizing phosphatidylserine during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiaochen -- Wu, Yi-Chun -- Fadok, Valerie A -- Lee, Ming-Chia -- Gengyo-Ando, Keiko -- Cheng, Li-Chun -- Ledwich, Duncan -- Hsu, Pei-Ken -- Chen, Jia-Yun -- Chou, Bin-Kuan -- Henson, Peter -- Mitani, Shohei -- Xue, Ding -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645848" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Caenorhabditis elegans/cytology/embryology/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/*metabolism ; *Cytoskeletal Proteins ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Membrane Proteins/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/genetics/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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  • 7
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    Notch-mediated restoration of regenerative potential to aged muscle (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: A hallmark of aging is diminished regenerative potential of tissues, but the mechanism of this decline is unknown. Analysis of injured muscle revealed that, with age, resident precursor cells (satellite cells) had a markedly impaired propensity to proliferate and to produce myoblasts necessary for muscle regeneration. This was due to insufficient up-regulation of the Notch ligand Delta and, thus, diminished activation of Notch in aged, regenerating muscle. Inhibition of Notch impaired regeneration of young muscle, whereas forced activation of Notch restored regenerative potential to old muscle. Thus, Notch signaling is a key determinant of muscle regenerative potential that declines with age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conboy, Irina M -- Conboy, Michael J -- Smythe, Gayle M -- Rando, Thomas A -- NRSA-AG05902/NR/NINR NIH HHS/ -- R01-NS36409/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1575-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305-5235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645852" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Calcium-Binding Proteins ; Cell Count ; Cell Differentiation ; Cell Division ; Cell Separation ; Culture Techniques ; Hindlimb ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Male ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/cytology/injuries/*physiology ; Myoblasts/*physiology ; Nerve Tissue Proteins/metabolism ; Receptor, Notch1 ; *Receptors, Cell Surface ; Recombinant Fusion Proteins/metabolism ; *Regeneration ; Satellite Cells, Skeletal Muscle/*physiology ; Signal Transduction ; *Transcription Factors ; Up-Regulation
    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. 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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  • 9
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    Cell biology. Eat me or die (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savill, John -- Gregory, Chris -- Haslett, Chris -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1516-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Centre for Inflammation Research, University of Edinburgh College of Medicine and Veterinary Medicine, Edinburgh EH8 9AG, UK. j.savill@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Autoimmunity ; Brain/abnormalities/embryology ; Caenorhabditis elegans/embryology/metabolism ; Caenorhabditis elegans Proteins/metabolism ; Cell Division ; Cytoskeleton/metabolism ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Embryonic and Fetal Development ; Inflammation ; Lung/embryology/metabolism ; Macrophages/physiology ; Mice ; Phagocytes/*physiology ; *Phagocytosis ; Phenotype ; Phosphatidylserines/metabolism ; Receptors, Cell Surface/*metabolism ; Respiratory Insufficiency/etiology ; 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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  • 10
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    Mutation of MEF2A in an inherited disorder with features of coronary artery disease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-03
    Description: The early genetic pathway(s) triggering the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI) remain largely unknown. Here, we describe an autosomal dominant form of CAD/MI (adCAD1) that is caused by the deletion of seven amino acids in transcription factor MEF2A. The deletion disrupts nuclear localization of MEF2A, reduces MEF2A-mediated transcription activation, and abolishes synergistic activation by MEF2A and by the transcription factor GATA-1 through a dominant-negative mechanism. The MEF2A protein demonstrates strong expression in the endothelium of coronary arteries. These results identify a pathogenic gene for a familial vascular disease with features of CAD and implicate the MEF2A signaling pathway in the pathogenesis of CAD/MI.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618876/" 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/PMC1618876/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lejin -- Fan, Chun -- Topol, Sarah E -- Topol, Eric J -- Wang, Qing -- R01 HL065630/HL/NHLBI NIH HHS/ -- R01 HL066251/HL/NHLBI NIH HHS/ -- R01 HL65630/HL/NHLBI NIH HHS/ -- R01 HL66251/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645853" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amino Acid Sequence ; Animals ; Arteries/metabolism ; Base Sequence ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 15/genetics ; Coronary Artery Disease/*genetics/metabolism ; Coronary Vessels/metabolism ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Dimerization ; Endothelium, Vascular/metabolism ; Erythroid-Specific DNA-Binding Factors ; Female ; Fluorescent Antibody Technique ; GATA1 Transcription Factor ; Gene Expression ; Genes, Dominant ; Genetic Linkage ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; MADS Domain Proteins ; MEF2 Transcription Factors ; Male ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth/cytology/metabolism ; Myocardial Infarction/*genetics/metabolism ; Myogenic Regulatory Factors ; Pedigree ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Protein Transport ; Rats ; Risk Factors ; *Sequence Deletion ; Signal Transduction ; Transcription Factors/chemistry/*genetics/metabolism ; Transcriptional Activation
    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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