BCL-2 family: regulators of cell death
DT Chao, SJ Korsmeyer - Annual review of immunology, 1998 - annualreviews.org
DT Chao, SJ Korsmeyer
Annual review of immunology, 1998•annualreviews.org▪ 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-XL,
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 …
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-XL,
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 …
▪ 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-XL, 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-XL display a reciprocal pattern of expression during lymphocyte development. Gain- and loss-of-function models revealed stage-specific roles for BCL-2 and BCL-XL. 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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