ABSTRACT

The cell death is a natural physiological process that occurs in every living organism. It is clear that programmed cell death - apoptosis - is an important mechanism maintaining cell number in a multicellular organism. This review summarises recent progress in the field of apoptosis. Extracellular signals, such as various growth factors and antigene Fas ligand can trigger apoptosis via cell surface receptors. Within the cell the tumor supressor gene p53 and oncogenes c-myc, c-fos and c-jun tend to activate apoptosis, while other genes such as most members of the bcl-2 family, tend to supress it. Many of these signals regulate a family of cysteine proteases - related to interleukine lp converting enzyme (ICE) - caspases - which play a crucial role in apoptosis. Many factors that affect apoptosis also affect the cell cycle. For example, p53 appears to be an important mediator of both apoptosis and cycle arrest. If DNA damage is repaired during cycle arrest, the cell survives. Special attention is paid to the abnormalities in the regulation of apoptosis that may contribute to different pathogenic processes.