Program in Molecular Medicine
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
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.
Rights and Permissions
Citation: Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15759-64. Epub 2007 Sep 24. Link to article on publisher's site
Publisher PDF posted as allowed by the publisher's author rights policy at http://www.pnas.org/site/aboutpnas/authorfaq.xhtml.
AP1, cJun, cell cycle
Das, Madhumita; Jiang, Feng; Sluss, Hayla Karen; Zhang, Chao; Shokat, Kevan M.; Flavell, Richard A.; and Davis, Roger J., "Suppression of p53-dependent senescence by the JNK signal transduction pathway" (2007). Open Access Articles. Paper 1354.