The bcl-2 product is considered to act as an inhibitor of apoptosis. bcl-2 expression is inhibited in germinal centers where apoptosis forms part of B cell production pathway. Reactive follicles show no staining for bcl-2, where as the cells in neoplastic follicles exhibit membrane staining.
Note: Not all species have been tested for usefulness with this product. Only those species listed have been tested. We cannot make any guarantees about additional reactivities which may or may not occur.
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Products are guaranteed for 6 months from date of receipt, except for peptides and proteins which are guaranteed for 3 months.
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.