Biochemistry, molecular genetics, and biology glossary terms for Companion Sites.


Programmed cell death (PCD) or cellular death-by-suicide is part of normal development, and is termed apoptosis. PCD is a part of normal cell turnover and tissue homeostasis, and it plays a significant role in embryogenesis, induction and maintenance of immune tolerance, development of the nervous system, and atrophy of endocrine-dependent tissue.

Signals from tumor suppressors such as APC, CBFA2T3, FAS gene, Hsp90, MDM2, p53, PTEN, TP53, Wnt prevent the uncontrolled proliferation characteristic of cancers by inducing apoptosis.

PCD is initiated via the death receptor pathway or the mitochondrial pathway, which lead to the activation of an initiator caspase, which in turn initiates a proteolytic cascade, ultimately leading to apoptotic cell death. Death receptors include the TNF-R (tumour necrosis factor receptors) and Fas receptor families (FADD). Activation of death receptors by binding of ligands such as TNF-α and CD-95L (FasL) leads to caspase-8 activity. Players in the mitochondrial pathway include members of the Bcl-2 family, which regulate the release, through the mitochondrial PT pore, of pro-apoptotic substances such as AIF, Endonuclease G, Smac/DIABLO and cytochrome C. Mitochondrial efflux of cytochrome-c drives generation of the apoptosome (apoptotic body) in the cytoplasm, which in turn leads to caspase-9 activity.

Apoptosis (PCD) exhibits characteristic morphological changes, and is distinct from necrosis.

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