Abstract
As we have discussed here, investigation of signaling pathways through gp130 to the nucleus in cardiac myocytes should uncover novel mechanisms of cardiac muscle growth and development. The dysregulation of this function caused by altered expression and/or altered function of gp130 may lead to pathological changes in cardiac myocytes. This is supported by findings in gp130 null mutants and the gp130-activated mouse model.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antigens, CD / physiology*
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Cardiomegaly / metabolism
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Cells, Cultured
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Cytokine Receptor gp130
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Membrane Glycoproteins / physiology*
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Mice
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Mitogen-Activated Protein Kinase 1
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Myocardium / cytology
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Myocardium / metabolism*
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Protein-Tyrosine Kinases / metabolism
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Receptors, Cytokine / physiology*
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Signal Transduction / physiology*
Substances
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Antigens, CD
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Il6st protein, mouse
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Membrane Glycoproteins
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Receptors, Cytokine
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Cytokine Receptor gp130
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Protein-Tyrosine Kinases
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Calcium-Calmodulin-Dependent Protein Kinases
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Mitogen-Activated Protein Kinase 1