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The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Transcription Factor ATF2 Regulation by the JNK Signal Transduction Pathway

Gupta, Shashi, Campbell, Debra, Dérijard, Benoit, Davis, Roger J.·1995·Science
DOI 10.1126/science.7824938
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Abstract

Treatment of cells with pro-inflammatory cytokines or ultraviolet radiation causes activation of the c-Jun NH 2 -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 NH 2 -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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Research works printed but not linked: 34

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Metadata

Authors
Gupta, S., Campbell, D., Dérijard, B., & Davis, R. J.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1995-01-20
Volume
267
Issue
5196
Pages
389-393
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.7824938
OpenAlex
W1984665850
Cited by
1,438
References
5
FWCI
42.99
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Transcription Factor ATF2 Regulation by the JNK Signal Transduction Pathway. https://app.cochat.ai/papers/10.1126/science.7824938
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Gupta, S., Campbell, D., Dérijard, B., & Davis, R. J. (1995). Transcription Factor ATF2 Regulation by the JNK Signal Transduction Pathway. Science. https://doi.org/10.1126/science.7824938

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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