Author Name: Keith Howell

Category Name: Medical science

Description:

In highly organized biological systems like multicellular organisms, tight regulation of growth and death is imminent. If cells are no longer required, they commit suicide by activating an intracellular death program. This method of programmed cell death is called apoptosis (from Ancient Greek á¼€πÏŒπτωσις "falling off"). Apoptosis is an energy-dependent biochemical processes characterized by distinct morphological features including cell shrinkage, nuclear fragmentation, chromatin condensation and membrane blebbing. It is a vital component of normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death, among others.
Because apoptosis cannot stop once it has begun, it is a highly regulated process. Apoptosis can be initiated through one of two pathways. In the intrinsic pathway the cell kills itself because it senses cell stress that results in activation of one or more members of BH3-only family of proteins.  In the extrinsic pathway the cell kills itself because of signals from other cells as a result of binding extracellular death ligands (such as FasL or tumour necrosis factor-alpha, TNF alpha). Both pathways induce cell death by activating caspases, which are proteases, or enzymes that degrade proteins. The two pathways activate initiator caspases (caspase 2, caspase 8 and caspase 9), which then activate executioner caspase (caspase 3, caspase 6 and caspase 7) that will kill the cell by degrading proteins indiscriminately. Defective apoptosis pathways can result in a wide variety of diseases including autoimmune disorders, neurodegenerative diseases, and many types of cancer.

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Media Contact:

Kieth Howell
Journal Manager
Journal of Cell signaling
Email: cellsignaling@peerjournal.org