Anti-Bcl-2, clone BL-2

0.5mg/ml with 1% BSA and 0.01% sodium azide if reconstituted with 0.2ml sterile 1XPBS. Immunoreactive BCL2 protein was detected in the neoplastic cells of almost all follicular lymphomas whereas no BCL2 protein was detected in follicles affected by nonneoplastic processes or in normal lymphoid tissue. Every tumor with molecular-genetic evidence of t(14,18) translocation expressed detectable levels of the protein, regardless of whether the breakpoint was located in or at a distance from the gene. Overexpression blocks the apoptotic death of a pro-B-lymphocyte cell line. Protein function: 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). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed:17418785). [The UniProt Consortium]