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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Cell Metab. 2009 Mar;9(3):277–286. doi: 10.1016/j.cmet.2009.01.006

Figure 5.

Figure 5

CREB stimulates expression of the transcriptional repressor ATF3 in adipose under obese conditions. A. Results from gene profiling studies showing genes induced 2-fold or greater in primary adipocytes following exposure to FSK and in WAT harvested from high fat diet (HFD) relative to normal chow fed mice. Presence of conserved CREB binding site (CRE) and TATA box indicated. B. Top left, relative ATF3 mRNA amounts in WAT from lean and ob/ob mice. Top right, effect of normal chow (NC) and high fat diet feeding (HFD) on ATF3 protein amounts in white adipose from wild-type mice. Bottom, relative ATF3 mRNA (left) and protein (right) amounts in WAT from F-ACREB ob/ob mice compared to control ob/ob animals. C. Q-PCR analysis of ATF3 mRNA in HEK293T cells (top) and in cultured primary adipocytes of ob/ob mice (bottom) following exposure to forskolin. Effect of ACREB expression, either acutely through adenoviral infection (ob Ad-ACREB), or chronically in cells from ACREB transgenic mice (tg ob) indicated. D. Chromatin Immunoprecipitation (ChIP) assay of subcutaneous or gonadal WAT showing CREB occupancy over the ATF3 promoter in vivo. CREB binding to positive control (FDPS) and negative control (actin) promoters shown for comparison. Relative recovery of ATF3 promoter from immunoprecipitates of CREB or non-specific IgG also indicated. Position of CREB binding site and TATA box relative to transcription start site on the ATF3 promoter shown.