Send to

Choose Destination
Oncogene. 2002 Apr 4;21(15):2441-5.

Differential effects of JNK1 and JNK2 on signal specific induction of apoptosis.

Author information

Research Institute of Molecular Pathology (IMP), Dr. Bohrgasse 7, A-1030 Vienna, Austria.


The c-Jun N-terminal kinases (JNKs) are activated by a variety of stress inducing agents and are thought to regulate apoptosis in a cell type and signal-specific manner. We have used fibroblasts lacking JNK1 or JNK2 to define their roles in response to different stress signals. Lack of JNK1 results in reduced c-Jun phosphorylation and resistance to UV-induced cell death. JNK2 deficient cells show increased sensitivity to UV irradiation which correlates with elevated and sustained phosphorylation of JNK1 and c-Jun. On the contrary, both Jnk1-/- and Jnk2-/- cells were more sensitive to tumor necrosis factor - alpha (TNF-alpha) and sorbitol-induced cell death. Treatment of Jnk1-/- cells with these reagents resulted in reduced JNK activity and a concomitant reduction of c-Jun phosphorylation, suggesting that phosphorylation of c-Jun does not influence TNF-alpha and sorbitol-induced apoptosis in fibroblasts. Moreover, both JNK1 and JNK2 appear to negatively regulate apoptosis independent of c-Jun phosphorylation. These data provide genetic evidence that although the JNK pathway is activated by a plethora of signals, it is required only for the induction of UV-induced cell death in a c-Jun phosphorylation-dependent manner, but not for TNF-alpha and sorbitol-induced apoptosis.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center