期刊
CELL RESEARCH
卷 18, 期 9, 页码 900-910出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cr.2008.75
关键词
GIDE; apoptosis; E3 ligase; mitochondria; caspase; JNK
类别
资金
- Hi-Tech Research and Development Program of China [2006AA02A306]
- Chinese 111 project [B06018]
- National Institutes of Health [CA108771]
- NATIONAL CANCER INSTITUTE [R01CA108771] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI018785, P01AI022295] Funding Source: NIH RePORTER
Here, we report the identification of GIDE, a mitochondrially located E3 ubiquitin ligase. GIDE contains a C-terminal RING finger domain, which is mostly conserved with those of the IAP family members and is required for GIDE's E3 ligase activity. Overexpression of GIDE induces apoptosis via a pathway involving activation of caspases, since caspase inhibitors, XIAP and an inactive mutant of caspase-9 block GIDE-induced apoptosis. GIDE also activates JNK, and blockage of JNK activation inhibits GIDE-induced release of cytochrome c and Smac as well as apoptosis, suggesting that JNK activation precedes release of cytochrome c and Smac and is required for GIDE-induced apoptosis. These pro-apoptotic properties of GIDE require its E3 ligase activity. When somewhat over-or underexpressed, GIDE slows or accelerates cell growth, respectively. These pro-apoptotic or growth inhibition effects of GIDE may account for its absence in tumor cells.
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