Main Article Content
Apoptosis (programmed cell death) is required for the removal of infected, damaged or unwanted cells. Inadequate cell death is a major contributing factor to tumorigenesis, while excess cell death contributes to neurodegeneration and autoimmune diseases.
Current investigations suggest the mechanisms by which Bcl-2 might prevent cell death. Bcl-2 family members mediate anti-apoptotic signals in a wide variety of human cell systems. Bcl-2 protein family, through its role in the regulation of apoptotic pathways, is possibly related to cancer pathophysiology. This review article discribes some pathways how apoptotic cell death is controlled by this protein family.