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Suppression of p53-dependent senescence by the JNK signal transduction pathway.

ABSTRACT: The JNK signaling pathway is implicated in the regulation of the AP1 transcription factor and cell proliferation. Here, we examine the role of JNK by using conditional and chemical genetic alleles of the ubiquitously expressed murine genes that encode the isoforms JNK1 and JNK2. Our analysis demonstrates that JNK is not essential for proliferation. However, JNK is required for expression of the cJun and JunD components of the AP1 transcription factor, and JNK-deficient cells exhibit early p53-dependent senescence. These data demonstrate that JNK can act as a negative regulator of the p53 tumor suppressor.

SUBMITTER: Das M

PROVIDER: S-EPMC2000443 | biostudies-literature | 2007 Oct

REPOSITORIES: biostudies-literature

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Suppression of p53-dependent senescence by the JNK signal transduction pathway.

Das Madhumita M Jiang Feng F Sluss Hayla K HK Zhang Chao C Shokat Kevan M KM Flavell Richard A RA Davis Roger J RJ

Proceedings of the National Academy of Sciences of the United States of America 20070924 40

The JNK signaling pathway is implicated in the regulation of the AP1 transcription factor and cell proliferation. Here, we examine the role of JNK by using conditional and chemical genetic alleles of the ubiquitously expressed murine genes that encode the isoforms JNK1 and JNK2. Our analysis demonstrates that JNK is not essential for proliferation. However, JNK is required for expression of the cJun and JunD components of the AP1 transcription factor, and JNK-deficient cells exhibit early p53-de ...[more]

PMID: 17893331

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