BCL2 is a protein that regulates apoptosis by controlling mitochondrial permeability and the release of cytochrome c1. Overexpression of BCL2 promotes cell survival by inhibiting apoptosis, which has been found to be associated with poor prognosis in breast, prostate, ovarian, endometrial and colon cancers. In normal lymphoid tissues, BCL2 antibodies label many cells in the small B-lymphocytes and T-cell regions of the mantle. BCL2 has great value in distinguishing the reactivity and tumor follicular proliferation in lymphoid injury.
Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).
BCL2 (BCL2 Apoptosis Regulator) is a Protein Coding gene. Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). Also acts as an inhibitor of autophagy: interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function. May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release.
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