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Molecular and Cellular Biology, July 2009, p. 3657-3664, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.01640-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Caspase-10-Mediated Heat Shock Protein 90β Cleavage Promotes UVB Irradiation-Induced Cell Apoptosis{triangledown}

Hehua Chen,1,{dagger} Yan Xia,1,{dagger} Dexing Fang,1 David Hawke,2 and Zhimin Lu1,3,4*

Brain Tumor Center and Department of Neuro-Oncology,1 Department of Molecular Pathology,2 Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030,3 University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas 770304

Received 21 October 2008/ Returned for modification 21 November 2008/ Accepted 10 April 2009

Heat shock protein 90β (Hsp90β) is involved in many cellular functions. However, the posttranslational modification of Hsp90β, especially in response to apoptotic stimulation, is not well understood. In this study, we found that Hsp90β was cleaved by activated caspase-10 under UVB irradiation. Caspase-10 activation, in turn, depended on caspase-8, which cleaved caspase-10 directly. Autocrine secretion of FAS ligand and upregulated FAS expression induced by UVB irradiation contributed to activation of caspase-10, which cleaved Hsp90β at D278, P293, and D294. The downregulation of Hsp90β mediated by caspase-8-dependent caspase-10 activation promoted UVB-induced cell apoptosis.

* Corresponding author. Mailing address: Department of Neuro-Oncology, Unit 1002, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030. Phone: (713) 834-6231. Fax: (713) 834-6230. E-mail: zhiminlu{at}mdanderson.org

{triangledown} Published ahead of print on 20 April 2009.

{dagger} H.C. and Y.X. made equal contributions to this work.

Molecular and Cellular Biology, July 2009, p. 3657-3664, Vol. 29, No. 13
0270-7306/09/$08.00+0     doi:10.1128/MCB.01640-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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