Deletion of SOCS7 leads to enhanced insulin action and enlarged islets of Langerhans
J. Clin. Invest. Alexander S. Banks, et al. 115:2462 doi:10.1172/JCI23853 [Go to this article.]

Figure 5
Resistance to stimulation-induced IRS1 degradation and increased adipogenesis in Socs7-deficient cells. (A) Socs7+/+ (WT) or Socs7 –/ – (KO) MEF cells were serum starved for 14–16 hours before a 30-minute pretreatment without (lanes 1, 2, 5, and 6) or with (lanes 3, 4, 7, and 8) lactacystin (Lact), a proteasome inhibitor. Cells were then stimulated with 10 nM IGF-1 for 6 hours. Immunoblotting for IRS1 was performed, followed by membrane stripping and reprobing with anti-p85 as a protein loading control. (B) Wild-type and Socs7-, Socs1-, and Socs3-deficient MEF cells were subjected to adipocyte differentiation (see Methods). Differentiation was scored either by staining for oil red O to measure triglyceride accumulation or by (C) Q-PCR for Pparg (normalized to Hprt) relative to 3T3-L1 adipocytes during differentiation.