Journal
MOLECULAR CARCINOGENESIS
Volume 46, Issue 8, Pages 591-598Publisher
WILEY-LISS
DOI: 10.1002/mc.20348
Keywords
JNK; MAP kinase; cancer; signal transduction
Categories
Funding
- NCI NIH HHS [R01 CA077646-09, CA88961, R01 CA081064-08, CA77646, P01 CA027502-270022, R37 CA081064, R01 CA111356-03, P01 CA088961-020003, R01 CA111356, CA27502, P01 CA088961, CA81064, CA11135, P01 CA027502, R01 CA081064, R01 CA077646] Funding Source: Medline
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The JNK proteins are activated by multiple and diverse stimuli, leading to varied and seemingly contradictory cellular responses. In particular, JNKs have been reported to have a role in the induction of apoptosis, but have also been implicated in enhancing cell survival and proliferation. Thus the JNK proteins seem to represent an archetype of contrariety of intracellular signaling. The opposing roles of JNKs have been attributed to the observation that JNKs activate different substrates based on specific stimulus, cell type or temporal aspects. Because of their analogous expression in apparently almost every tissue, JNK1 and JNK2 have most often been considered to have overlapping or redundant functions. In spite of this assessment, research evidence suggests that the functions of JNKs should be addressed in a manner that differentiates between their precise contributions. Specifically in this review, we examine evidence regarding whether the JINKs proteins might play distinctive roles in cellular processes associated with carcinogenesis. (c) 2007 Wiley-Liss, Inc.
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