期刊
BIOCHEMICAL JOURNAL
卷 430, 期 -, 页码 199-205出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20100814
关键词
cancer therapy; inhibitor of apoptosis (IAP); mitochondrion; nuclear factor kappa B (NF-kappa B); survivin
资金
- National Institutes of Health [CA118005, CA90917, CA78810, HL54131]
- NATIONAL CANCER INSTITUTE [R01CA078810, R01CA118005, R01CA090917] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL054131, R37HL054131] Funding Source: NIH RePORTER
From the realization that cell number homoeostasis is fundamental to the biology of all metazoans, and that deregulation of this process leads to human diseases, enormous interest has been devoted over the last two decades to map the requirements of cell death and cell survival. This effort has led to tangible progress, and we can now chart with reasonable accuracy complex signalling circuitries controlling cell-fate decisions. Some of this knowledge has translated into novel therapeutics, and the outcome of these strategies, especially in cancer, is eagerly awaited. However, the function of cell-death modifiers have considerably broadened over the last few years, and these molecules are increasingly recognized as arbiters of cellular homoeostasis, from cell division, to intracellular signalling to cellular adaptation. This panoply of functions is best exemplified by members of the IAP (inhibitor of apoptosis) gene family, molecules originally narrowly defined as endogenous caspase inhibitors: but now firmly positioned at the crossroads of multiple normal and transformed cellular responses.
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