Article
- The EMBO Journal (2005) 24, 4237 - 4246
- doi:10.1038/sj.emboj.7600882
Published online: 24 November 2005
Subject Category:
-Arrestin2 functions as a phosphorylation-regulated suppressor of UV-induced NF-
B activation
Bing Luan1, Zhenning Zhang1, Yalan Wu1, Jiuhong Kang1 and Gang Pei1
- Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and Graduate School of the Chinese Academy of Sciences, Shanghai, People's Republic of China
Correspondence to:
Gang Pei, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, People's Republic of China. Tel.: +86 21 5492 1371; Fax: +86 21 5492 1011; E-mail: gpei@sibs.ac.cn
Received 4 July 2005; Accepted 31 October 2005
Abstract
NF-
B activation is an important mechanism of mammalian UV response to protect cells. UV-induced NF-B activation depends on the casein kinase II (CK2) phosphorylation of IB
at a cluster of C-terminal sites, but how it is regulated remains unclear. Here we demonstrate that 
-arrestin2 can function as an effective suppressor of UV-induced NF-B activation through its direct interaction with IB. CK2 phosphorylation of -arrestin2 blocks its interaction with IB and abolishes its suppression of NF-B activation, indicating that the -arrestin2 phosphorylation is critical. Moreover, stimulation of 2-adrenergic receptors, a representative of G-protein-coupled receptors in epidermal cells, promotes dephosphorylation of -arrestin2 and its suppression of NF-B activation. Consequently, the -arrestin2 suppression leads to promotion of UV-induced cell death, which is also under regulation of -arrestin2 phosphorylation. Thus, -arrestin2 is identified as a phosphorylation-regulated suppressor of UV response and this may play a functional role in the response of epidermal cells to UV.
Keywords:
- -arrestin2,
- CK2,
- NF-B
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