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Cyclic AMP stimulates somatostatin gene transcription by phosphorylation of CREB at serine 133.

In this paper, we demonstrate that phosphorylation of CREB at Ser-133 is induced 6-fold in vivo, following treatment of PC12 cells with forskolin. By contrast, no such induction was observed in the kinase A-deficient PC12 line A126-1B2 (A126). Using F9 teratocarcinoma cells, which are unresponsive to cAMP, we initiated a series of transient expression experiments to establish a causal link between phosphorylation of CREB and trans-activation of cAMP-responsive genes. Inactivating the kinase A phosphorylation site by in vitro mutagenesis of the cloned CREB cDNA at Ser-133 completely abolished CREB transcriptional activity. As CREB mutants containing acidic residues in place of the Ser-133 phosphoacceptor were also transcriptionally inactive, these results suggest that phosphorylation of CREB may stimulate transcription by a mechanism other than by simply providing negative charge.

Pubmed ID: 2573431


  • Gonzalez GA
  • Montminy MR



Publication Data

November 17, 1989

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM 37828

Mesh Terms

  • Adrenal Gland Neoplasms
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Cell Line
  • Colforsin
  • Cyclic AMP
  • Cyclic AMP Response Element-Binding Protein
  • DNA-Binding Proteins
  • Genes
  • Molecular Sequence Data
  • Mutation
  • Peptide Mapping
  • Pheochromocytoma
  • Phosphorylation
  • Rats
  • Serine
  • Somatostatin
  • Transcription, Genetic
  • Transfection