Abstract
Various intracellular or intercellular stimuli have been associated with the development of cardiac cell hypertrophy. However, the mechanisms underlying this association are not completely understood. In a previous study we determined that ZAK mRNA expression is abundant in heart. ZAK is a mitogen-activated protein kinase kinase kinase (MAP3K) that activates the stress-activated protein kinase/c-jun N-terminal kinase pathway and activates NF-kappaB. We, therefore, investigated the potential involvement of ZAK (which in cultured H9c2 cardiomyoblast cell is a positive mediator of cell hypertrophy). Our results showed that the expression of a wild-type form of ZAK induces the characteristic hypertrophic growth features, including increased cell size, elevated atrial natriuretic factor expression, and increased actin fiber organization.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / chemistry
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Actins / metabolism
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Amino Acid Motifs
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Animals
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Atrial Natriuretic Factor / biosynthesis*
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Blotting, Western
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Cell Cycle
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Cell Cycle Proteins / metabolism
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Cell Line
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Cells, Cultured
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Cyclin-Dependent Kinase Inhibitor p21
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Disulfides / chemistry
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Enzyme Activation
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Gene Expression Regulation
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Genetic Vectors
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Humans
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Immunoprecipitation
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JNK Mitogen-Activated Protein Kinases / chemistry
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Leucine / chemistry
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MAP Kinase Kinase Kinases / metabolism
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MAP Kinase Signaling System*
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Mutation
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Myocytes, Cardiac / metabolism*
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NF-kappa B / metabolism
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Protein Kinases / metabolism
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Protein Kinases / physiology*
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Protein Structure, Tertiary
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Rats
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Time Factors
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Transfection
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Up-Regulation
Substances
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Actins
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CDKN1A protein, human
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Cdkn1a protein, rat
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Cell Cycle Proteins
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Cyclin-Dependent Kinase Inhibitor p21
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Disulfides
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NF-kappa B
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Atrial Natriuretic Factor
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Protein Kinases
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JNK Mitogen-Activated Protein Kinases
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MAP Kinase Kinase Kinases
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MAP3K20 protein, human
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Leucine