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GH activates the c- fos  promoter by regulating multiple transcription factors. This study adds to our understanding of GH-regulated transcription by demonstrating that GH regulates the c- fos  cAMP-response element (CRE) and its binding protein, CREB. Activation of the c- fos  promoter by GH is impaired by expression of dominant-negative A-CREB. GH stimulates rapid and transient phosphorylation of CREB at Ser 133 (P-CREB), a critical site for transactivation by CREB, in 3T3-F442A preadipocytes. Mutation of this residue impairs GH-induced c- fos  expression, suggesting that phosphorylation of CREB at Ser 133 contributes to GH-induced c- fos  activation. The MEK inhibitor UO126 impaired the phosphorylation of CREB and that of C/EBPβ, suggesting that ERKs mediate the phosphorylation of both proteins. UO126, but not the protein kinase A inhibitor H89, blocked GH-induced c- fos  mRNA expression. A combination of CREB and C/EBPβ enhanced c- fos  promoter activation, and mutation of the CRE impaired the enhancement, as well as GH-stimulated c- fos  activation. GH treatment increased the occupancy of both endogenous phospho-CREB and phospho-C/EBPβ on the c- fos  promoter. The increases were impaired by UO126. The active P-CREB and P-C/EBPβ are induced by GH to occupy the same c- fos  promoter DNA, suggesting that they may participate in a GH-regulated complex on c- fos . These findings suggest that coordinated phosphorylation of CREB and C/EBPβ in response to GH is mediated by ERK1/2, and that the phosphorylated proteins are part of a regulatory complex that occupies c- fos   in vivo  to regulate c- fos  transcription cooperatively in response to GH.

Cooperative regulation of endogenous cAMP-response element binding protein and CCAAT/enhancer-binding protein β in GH-stimulated c-fos expression