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      BCL-2 family: regulators of cell death.

      1 ,

      Annual review of immunology

      Annual Reviews

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          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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          Author and article information

          Journal
          Annu Rev Immunol
          Annual review of immunology
          Annual Reviews
          0732-0582
          0732-0582
          1998
          : 16
          Affiliations
          [1 ] Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
          Article
          10.1146/annurev.immunol.16.1.395
          9597135
          0f84d4c7-2f7e-4d6f-ac1c-b0a6e85890ff

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