Abstract
c-Jun NH2-terminal kinase (JNK) was discovered almost 20 years ago as the protein kinase responsible for phosphorylating c-Jun at Ser-63 and Ser-73. These sites had previously been demonstrated to be essential for the stimulation of c-Jun activity and for cooperation with Ha-ras in oncogenic transformation. This led to the idea that JNK was a positive regulator of cellular transformation. However, the analysis of jnk gene deletion in various mouse models of cancer has produced conflicting findings, with some studies supporting the pro-oncogenic function of JNK and others providing evidence that JNK acts as a tumor suppressor. This review will discuss how these unexpected findings have increased our understanding of the role of JNK signaling in cancer and have provided a source of new working hypotheses. © The Author(s) 2013.
Original language | English |
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Pages (from-to) | 397-400 |
Number of pages | 3 |
Journal | Genes and Cancer |
Volume | 4 |
Issue number | 9-10 |
DOIs | |
Publication status | Published - Sept 2013 |
Keywords
- c-Jun
- cancer
- JNK
- MAPK
- MKK
- Ras