生物
细胞生物学
细胞凋亡
Bcl-2家族
程序性细胞死亡
半胱氨酸蛋白酶
磷酸化
同源(生物学)
功能(生物学)
信号转导
遗传学
基因
作者
Debra T. Chao,Stanley J. Korsmeyer
出处
期刊:Annual Review of Immunology
[Annual Reviews]
日期:1998-04-01
卷期号:16 (1): 395-419
被引量:1603
标识
DOI:10.1146/annurev.immunol.16.1.395
摘要
▪ Abstract An expanding family of BCL-2 related proteins share homology, clustered within four conserved regions, namely BCL-2 homology (BH1-4) domains, which control the ability of these proteins to dimerize and function as regulators of apoptosis. Moreover, BCL-X L , BCL-2, and BAX can form ion-conductive pores in artificial membranes. The BCL-2 family, comprised of both pro-apoptotic and anti-apoptotic members, acts as a checkpoint upstream of CASPASES and mitochondrial dysfunction. BID and BAD possess the minimal death domain BH3, and the phosphorylation of BAD connects proximal survival signals to the BCL-2 family. BCL-2 and BCL-X L display a reciprocal pattern of expression during lymphocyte development. Gain- and loss-of-function models revealed stage-specific roles for BCL-2 and BCL-X L . BCL-2 can rescue maturation at several points of lymphocyte development. The BCL-2 family also reveals evidence for a cell-autonomous coordination between the opposing pathways of proliferation and cell death.
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