Document Type
Article
Publication Date
5-26-2006
Abstract
Insulin receptor substrate (IRS)-1 is a key protein in insulin signaling. Several studies have shown that the expression of IRS-1 can be modulated by protein degradation via the proteasome and the degradation of IRS-1 can be related to insulin-resistant states. The degradation of IRS-1 has been shown to be induced by SOCS-1 and SOCS-3 via the ubiquitin pathway. The goal of our study was to determine if the induction of SOCS-3 correlated with increased IRS-1 degradation in cultured 3T3-L1 adipocytes. Interestingly, our studies have shown that there is little correlation between the induction in SOCS-3 expression and the degradation of IRS-1 in mature 3T3-L1 adipocytes. Our results clearly demonstrate that treatment with leukemia inhibitory factor (LIF) or cardiotrophin (CT)-1 strongly induces the expression of SOCS-3 in mature 3T3-L1 adipocytes, but does not affect the degradation of IRS-1. On the contrary, tumor necrosis factor (TNF) α and insulin, which very weakly induce SOCS-3 expression, have profound effects on IRS-1 degradation. In summary, our results indicate that the expression of SOCS-3 does not correlate with the degradation of IRS-1 proteins in fat cells. © 2006 Elsevier Inc. All rights reserved.
Publication Source (Journal or Book title)
Biochemical and Biophysical Research Communications
First Page
95
Last Page
98
Recommended Citation
He, F., & Stephens, J. (2006). Induction of SOCS-3 is insufficient to confer IRS-1 protein degradation in 3T3-L1 adipocytes. Biochemical and Biophysical Research Communications, 344 (1), 95-98. https://doi.org/10.1016/j.bbrc.2006.03.142