Suppression of p53-dependent senescence by the JNK signal transduction pathway
Authors
Das, MadhumitaJiang, Feng
Sluss, Hayla Karen
Zhang, Chao
Shokat, Kevan M.
Flavell, Richard A.
Davis, Roger J.
UMass Chan Affiliations
Program in Molecular MedicineDocument Type
Journal ArticlePublication Date
2007-10-02Keywords
AP1cJun
cell cycle
Biochemistry
Cell Biology
Cellular and Molecular Physiology
Molecular Biology
Metadata
Show full item recordAbstract
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.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 siteDOI
10.1073/pnas.0707782104Permanent Link to this Item
http://hdl.handle.net/20.500.14038/38481PubMed ID
17893331Related Resources
Link to Article in PubMedRights
Publisher PDF posted as allowed by the publisher's author rights policy at http://www.pnas.org/site/aboutpnas/authorfaq.xhtml.
ae974a485f413a2113503eed53cd6c53
10.1073/pnas.0707782104