TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28
| Autor: | Anton Wernig, Peter Storz, Gertraud Müller, Heike Döppler, Klaus Pfizenmaier |
|---|---|
| Jazyk: | angličtina |
| Předmět: |
Male
Time Factors medicine.medical_treatment Skeletal muscle Biochemistry Mice Structural Biology STAT5 Transcription Factor Myocyte Insulin Phosphorylation Cells Cultured STAT5 Mice Inbred BALB C biology NF-kappa B Caseins Cell Differentiation Milk Proteins DNA-Binding Proteins medicine.anatomical_structure Tumor necrosis factor alpha Signal Transduction medicine.medical_specialty Tumor necrosis factor Biophysics Myosins Insulin resistance Internal medicine Genetics medicine Animals Kinase activity Muscle Skeletal Phosphotyrosine Molecular Biology Tumor Necrosis Factor-alpha Cell Biology Receptor Cross-Talk medicine.disease IRS2 Receptor Insulin Enzyme Activation Insulin receptor Endocrinology biology.protein Trans-Activators |
| Zdroj: | FEBS Letters. (1-2):41-45 |
| ISSN: | 0014-5793 |
| DOI: | 10.1016/S0014-5793(98)01421-5 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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