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Transcription factor ATF2 regulation by the JNK signal transduction pathway.

Authors
  • Gupta, S
  • Campbell, D
  • Dérijard, B
  • Davis, R J
Type
Published Article
Journal
Science (New York, N.Y.)
Publication Date
Jan 20, 1995
Volume
267
Issue
5196
Pages
389–393
Identifiers
PMID: 7824938
Source
Medline
License
Unknown

Abstract

Treatment of cells with pro-inflammatory cytokines or ultraviolet radiation causes activation of the c-Jun NH2-terminal protein kinase (JNK). Activating transcription factor-2 (ATF2) was found to be a target of the JNK signal transduction pathway. ATF2 was phosphorylated by JNK on two closely spaced threonine residues within the NH2-terminal activation domain. The replacement of these phosphorylation sites with alanine inhibited the transcriptional activity of ATF2. These mutations also inhibited ATF2-stimulated gene expression mediated by the retinoblastoma (Rb) tumor suppressor and the adenovirus early region 1A (E1A) oncoprotein. Furthermore, expression of dominant-negative JNK inhibited ATF2 transcriptional activity. Together, these data demonstrate a role for the JNK signal transduction pathway in transcriptional responses mediated by ATF2.

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