期刊
SEMINARS IN CANCER BIOLOGY
卷 16, 期 3, 页码 193-202出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2006.03.003
关键词
14-3-3; apoptosis; survival signaling; BAD; JNK
类别
资金
- NCI NIH HHS [CA116676] Funding Source: Medline
- NIGMS NIH HHS [R01 GM53165] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA116676] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM053165] Funding Source: NIH RePORTER
The serine/threonine binding protein, 14-3-3, possesses a diverse array of client proteins. It is involved in the regulation of apoptosis through multiple interactions with proteins of the core mitochondrial machinery, pro-apoptotic transcription factors, and their upstream signaling pathways. 14-3-3 coordinates with survival kinases to inhibit multiple pro-apoptotic molecules. One prominent mechanism for the suppression of apoptosis is through 14-3-3-mediated sequestration of pro-apoptotic client proteins. On the other hand, cellular stresses appear to signal through the inhibition of 14-3-3 function to exert their pro-apoptotic effect. Global inhibition of 14-3-3/client protein interaction induces apoptosis, and stands as an attractive intervention in diseases involving overactive survival signaling pathways. Because dysregulation of 14-3-3 has been associated with poor survival of cancer patients, targeting 14-3-3 may provide a novel therapeutic approach for the treatment of cancer. (c) 2006 Elsevier Ltd. All rights reserved.
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