Mouse Anti- Bcl- 2- UNLB(0.1 mg)

Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems.² 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.³ 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, gamma-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. The monoclonal antibody 10C2 reacts with both mouse and rat Bcl-2.¹