Transcription factor ATF2 regulation by the JNK signal transduction pathway
S Gupta, D Campbell, B Derijard, RJ Davis - Science, 1995 - science.org
S Gupta, D Campbell, B Derijard, RJ Davis
Science, 1995•science.orgTreatment 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 …
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 …
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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