Abstract
Tumor necrosis factor (TNF) plays a central role in the state of insulin resistance leading to type II diabetes. We here describe the crosstalk of TNF with insulin signaling cascades in the mouse muscle cell line pmi28. TNF downregulated insulin induced insulin receptor kinase activity and insulin induced activation of the transcription factor STAT5. Our results provide evidence that the inhibitory crosstalk between TNF and insulin in skeletal muscle cells comprises an interference with the expression of STAT5 regulated genes which may play an important role in the manifestation and/or progression of insulin resistance in muscle cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Caseins / genetics
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Cell Differentiation
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Cells, Cultured
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DNA-Binding Proteins / metabolism*
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Enzyme Activation
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Insulin / pharmacology*
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Male
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Mice
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Mice, Inbred BALB C
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Milk Proteins*
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Muscle, Skeletal / cytology
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Muscle, Skeletal / metabolism*
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Myosins / analysis
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NF-kappa B / metabolism
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Phosphorylation / drug effects
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Phosphotyrosine / analysis
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Receptor Cross-Talk
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Receptor, Insulin / metabolism
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STAT5 Transcription Factor
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Signal Transduction*
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Time Factors
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Trans-Activators / metabolism*
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Tumor Necrosis Factor-alpha / pharmacology*
Substances
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Caseins
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DNA-Binding Proteins
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Insulin
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Milk Proteins
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NF-kappa B
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STAT5 Transcription Factor
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Trans-Activators
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Tumor Necrosis Factor-alpha
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Phosphotyrosine
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Receptor, Insulin
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Myosins