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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: Mol Cell Endocrinol. 2014 Aug 1;395(0):19–31. doi: 10.1016/j.mce.2014.07.020

Fig. 1.

Fig. 1

BCL6 and STAT5 occupy Socs2 DNA reciprocally in response to GH. (A) 3T3-F442A preadipocytes were treated with GH for 0, 0.5 or 48 h and ChIP was carried out using antibodies against BCL6, STAT5, STAT5a or STAT5b. ChIP DNA was probed with primers specific to the STAT5 occupancy sequence on the Socs2 promoter. IgG served as a negative control and 1% input was used as an internal control, in this and subsequent figures. Data are representative of at least two experiments. (B) 3T3-F442A preadipocytes and adipocytes were treated with GH for 0 and 24 h and ChIP was carried out using antibodies against BCL6, STAT5, and phosphorylated STAT5 (P-STAT5). ChIP DNA was probed with primers specific to the STAT5 occupancy sequence on the Socs2 promoter. (C) Male littermate mice were treated ip with GH (1.5 mg/kg in 48 h) (+) or vehicle (−). Liver was used for ChIP analysis using antibodies against BCL6, STAT5 or P-STAT5 and probed for Socs2 as above.