Description
Product Characteristics: Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems. It plays a key role in tissue and organ development as well as in adult tissues during cell turnover. Apoptosis can be induced by a variety of internal and external stimuli including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation and glucocorticoid treatment. Bcl-2 is a widely studied protein that has been shown to be a potent inhibitor of programmed cell death. It has been localized to the outer mitochondrial membrane, perinuclear membrane, and endoplasmic reticulum. Bcl-2 is expressed in memory and resting, or other long-lived lymphoid cells, follicular mantle cells, medullary thymocytes, and lymphomas. Germical center cells and cortical thymocytes are negative for Bcl-2. Upregulation of Bcl-2 prevents or delays apoptosis induced by a variety of stimuli, including growth factor deprivation, -irradiation, glucocorticoids, and chemotherapeutic agents. During lymphoid development, expression of the Bcl-2 protein appears to be regulated in a stage-specific manner, and is thought to be a survival signal for positive selection.
Target Information: This gene encodes 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, produced by alternate splicing, differ in their C-terminal ends. [provided by RefSeq, Jul 2008]