title: 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.
authors: Program in Molecular Medicine, Department of Cancer Cell Biology, and Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
authors: Madhumita
authors: M
authors: Das
authors: Feng
authors: F
authors: Jiang
authors: Hayla K
authors: HK
authors: Sluss
authors: Chao
authors: C
authors: Zhang
authors: Kevan M
authors: KM
authors: Shokat
authors: Richard A
authors: RA
authors: Flavell
authors: Roger J
authors: RJ
authors: Davis
mesh_terms: D000818:Animals; D002455:Cell Division; D016922:Cellular Senescence / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology / Q000201:enzymology; D016158:Genes, p53; D007700:Kinetics; D048670:MAP Kinase Kinase 4 / Q000235:genetics / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D048055:Mitogen-Activated Protein Kinase 8 / Q000172:deficiency / Q000235:genetics; D016133:Polymerase Chain Reaction; D011494:Protein Kinases / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
chemical_list: D016755:Proto-Oncogene Proteins c-jun; D016159:Tumor Suppressor Protein p53; D011494:Protein Kinases; D048055:Mitogen-Activated Protein Kinase 8; D048670:MAP Kinase Kinase 4