Journal
ONCOGENE
Volume 26, Issue 33, Pages 4842-4849Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1210287
Keywords
cytokines; vitamins; cancer; cell death; growth; suppression
Funding
- NCI NIH HHS [CA105005] Funding Source: Medline
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We have isolated a novel interferon (IFN)-retinoid regulated cell death regulatory protein genes associated with retinoid-IFN-induced mortality (GRIM)-19 earlier. To understand its mechanism of action, we have employed a yeast-two-hybrid screen and identified serine protease HtrA2 as its binding partner. GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. In the presence of GRIM-19, the HtrA2-driven destruction of the antiapoptotic protein X-linked inhibitor of apoptosis (XIAP) is augmented. These interactions were disrupted by an human herpes virus-8 (HHV-8)-coded oncoprotein, vIRF1, and conferred resistance to IFN/RA-induced cell death. These data show a critical role of HtrA2 in a cytokine-induced cell death response for the. rst time and its inhibition by a viral protein.
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