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Cellular growth inhibition by TGF‐β 1 involves IRS proteins
Author(s) -
Huang Shuan Shian,
Leal Sandra M.,
Chen Chun-Lin,
Liu I-Hua,
Huang Jung San
Publication year - 2004
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/j.febslet.2004.03.082
Subject(s) - growth inhibition , transforming growth factor , transfection , growth factor , microbiology and biotechnology , transforming growth factor beta , cell growth , phosphorylation , receptor , cell culture , chemistry , biology , biochemistry , genetics
In Mv1Lu cells, insulin partially reverses transforming growth factor‐β 1 (TGF‐β 1 ) growth inhibition in the presence of α5β1 integrin antagonists. TGF‐β 1 appears to induce phosphorylation of IRS‐2 in these cells; this is inhibited by a TGF‐β antagonist known to reverse TGF‐β growth inhibition. Stable transfection of 32D myeloid cells (which lack endogenous IRS proteins and are insensitive to growth inhibition by TGF‐β 1 ) with IRS‐1 or IRS‐2 cDNA confers sensitivity to growth inhibition by TGF‐β 1 ; this IRS‐mediated growth inhibition can be partially reversed by insulin in 32D cells stably expressing IRS‐2 and the insulin receptor (IR). These results suggest that growth inhibition by TGF‐β 1 involves IRS proteins.
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