UMMS Affiliation
Program in Molecular Medicine
Publication Date
2007-10-02
Document Type
Article
Disciplines
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
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.
Keywords
AP1, cJun, cell cycle
Rights and Permissions
Publisher PDF posted as allowed by the publisher's author rights policy at http://www.pnas.org/site/aboutpnas/authorfaq.xhtml.
DOI of Published Version
10.1073/pnas.0707782104
Source
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
Journal/Book/Conference Title
Proceedings of the National Academy of Sciences of the United States of America
Related Resources
PubMed ID
17893331
Repository Citation
Das M, Jiang F, Sluss HK, Zhang C, Shokat KM, Flavell RA, Davis RJ. (2007). Suppression of p53-dependent senescence by the JNK signal transduction pathway. Open Access Articles. https://doi.org/10.1073/pnas.0707782104. Retrieved from https://escholarship.umassmed.edu/oapubs/1354
Included in
Biochemistry Commons, Cell Biology Commons, Cellular and Molecular Physiology Commons, Molecular Biology Commons