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TNF inhibits insulin induced STAT5 activation in differentiated mouse muscle cells pmi28
Author(s) -
Storz Peter,
Döppler Heike,
Wernig Anton,
Pfizenmaier Klaus,
Müller Gertraud
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01421-5
Subject(s) - insulin resistance , crosstalk , insulin receptor , insulin , medicine , tumor necrosis factor alpha , endocrinology , insulin receptor substrate , skeletal muscle , irs2 , biology , myocyte , microbiology and biotechnology , chemistry , physics , optics
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.

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