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• W4417669 abstract "Research Article15 December 1994free access Altering the specificity of signal transduction cascades: positive regulation of c-Jun transcriptional activity by protein kinase A. T. Smeal T. Smeal Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Hibi M. Hibi Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Karin M. Karin Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author T. Smeal T. Smeal Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Hibi M. Hibi Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Karin M. Karin Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author Author Information T. Smeal1, M. Hibi1 and M. Karin1 1Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093. The EMBO Journal (1994)13:6006-6010https://doi.org/10.1002/j.1460-2075.1994.tb06946.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Protein phosphorylation is commonly used to modulate transcription factor activity. However, all existing genetic evidence for stimulation of transcription factor activity by phosphorylation rests on loss-of-function mutations. To demonstrate conclusively that phosphorylation of a transcription factor potentiates its transactivation potential in vivo, we constructed a c-Jun mutant that is phosphorylated by the cAMP-sensitive protein kinase A (PKA) instead of the UV- and Ras-responsive protein kinase JNK. The transcriptional activity of this mutant is enhanced by PKA, but not by JNK activation. These results provide a positive and conclusive proof that phosphorylation of c-Jun on a critical site (Ser73) located in its activation domain is directly responsible for enhancing its transactivation function. Previous ArticleNext Article Volume 13Issue 241 December 1994In this issue RelatedDetailsLoading ..." @default.
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