[Apoptosis: molecular mechanisms].

E Solary

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PubMed · 10101603

[Apoptosis: molecular mechanisms].

E Solary

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Abstract

Apoptosis is a genetically programmed cell death that is required for morphogenesis during embryogenic development and for tissue homeostasis in adult organisms. In most cases, apoptosis involves cytochrome c release from mitochondria. In the cytosol, cytochrome c combines with APAF-1 in the presence of ATP to activate caspase-9 that, in turn, activates effectors caspases such as caspase-3. Bcl-2 and related proteins control cytochrome c release from the mitochondria whereas IAP (for Inhibitor of APoptosis) molecules modulate the activity of caspases. Plasma membrane receptors such as Fas (CD95, APO-1), characterized by a so-called "death domain" in their cytoplasmic domain, can activate the caspase cascade through adaptator molecules such as FADD (Fas-Associated protein with a Death Domain). Dysregulation of the apoptotic machinery plays a role in the pathogenesis of various diseases and molecules involved in cell death pathways are potential therapeutic targets in immunologic, neurologic, cancer, infectious and inflammatory diseases.

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Animals Apoptosis Embryonic and Fetal Development Humans Mitochondria Models, Biological Morphogenesis English Abstract Journal Article Research Support, Non-U.S. Gov't Review

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E Solary. 1998. [Apoptosis: molecular mechanisms].. https://pubmed.ncbi.nlm.nih.gov/10101603/

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