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Sci. Signal., 25 November 2008
Vol. 1, Issue 47, p. ra14
[DOI: 10.1126/scisignal.1161938]

RESEARCH

Editor's Summary

A ROCK in Stressful Times
Exposure of cells to ultraviolet B (UVB) radiation results in damage to DNA and the generation of mutations that can give rise to unchecked cellular proliferation. Thus, it is critically important to the prevention of skin cancers that the response to UVB-induced damage is to trigger apoptosis in the affected cells. In UVB-exposed cells, activation of members of the mitogen-activated protein kinase (MAPK) family, such as c-Jun N-terminal kinase (JNK), mediates this apoptotic response, but how UVB radiation activates signaling pathways upstream of JNK is unclear. Ongusaha et al. now show that exposure of keratinocytes to UVB radiation activates Rho-associated kinase 1 (ROCK1), which phosphorylates and activates the scaffold protein JNK-interacting protein 3 (JIP-3), which in turn recruits and activates JNK. Mice deficient in ROCK1 failed to mount as efficient an apoptotic response to UVB irradiation as did their wild-type counterparts, suggesting that ROCK1 is a critical early player in the response to UVB irradiation.

Citation: P. P. Ongusaha, H. H. Qi, L. Raj, Y.-B. Kim, S. A. Aaronson, R. J. Davis, Y. Shi, J. K. Liao, S. W. Lee, Identification of ROCK1 as an Upstream Activator of the JIP-3 to JNK Signaling Axis in Response to UVB Damage. Sci. Signal. 1, ra14 (2008).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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S. W. Lee, P. P. Ongusaha, and A. M. VanHook (2008)
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