Survivin and IAP proteins in cell-death mechanisms.
Survivin and IAP proteins in cell-death mechanisms.
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DOI：
10.1042/bj20100814
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发表时间：
2010-09-01
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影响因子：
--
通讯作者：
Altieri DC
中科院分区：
文献类型：
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作者：
Altieri DC
由于认识到细胞数量稳态是所有后生动物生物学的基础，并且这一过程的失调会导致人类疾病，因此在过去的二十年中人们对绘制细胞死亡和细胞生存的要求产生了极大的兴趣。这项努力取得了切实的进展，我们现在可以以合理的精度绘制控制细胞命运决定的复杂信号电路。其中一些知识已转化为新的治疗方法，人们热切期待这些策略的结果，特别是在癌症方面。然而，在过去几年中，细胞死亡调节剂的功能已大大扩展，并且这些分子越来越多地被认为是细胞稳态的仲裁者，从细胞分裂到细胞内信号传导，再到细胞适应。细胞凋亡抑制剂 (IAP) 基因家族的成员最能体现这种全部功能，这些分子最初被狭义地定义为内源性半胱天冬酶抑制剂，但现在牢牢地定位在多种正常和转化细胞反应的十字路口。
From the realization that cell number homeostasis 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 past 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 signaling 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 past few years, and these molecules are increasingly recognized as arbiters of cellular homeostasis, from cell division, to intracellular signaling, to cellular adaptation. This panoply of functions is best exemplified by members of the Inhibitor of Apoptosis (IAP) gene family, molecules originally narrowly defined as endogenous caspase inhibitors, but now firmly positioned at the crossroads of multiple normal and transformed cellular responses.