NDLI: Integration of apoptosis and metabolism.

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Integration of apoptosis and metabolism.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yi, C. H. Vakifahmetoglu-Norberg, H. Yuan, J.
Description	Country affiliation: United States Author Affiliation: Yi CH ( Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.)
Abstract	Apoptotic resistance is a hallmark of human cancers. Recent advances have contributed to our understanding of the molecular mechanisms that intimately integrate cell metabolism and apoptosis. Coordinated activation of the proapoptotic Bcl-2 family and the caspase family during apoptosis often leads to permeabilization of the mitochondrial outer membrane and release of multiple enzymes that normally function in regulating energy production and metabolism. The roles of these metabolic enzymes in promoting caspase activation demonstrate a primordial need to couple apoptotic cell death and metabolic catastrophe during cellular destruction. The Bcl-2 family also directly interacts with the multiple metabolic regulators to protect or promote mitochondrial damage during apoptosis. However, the integration of metabolism and apoptosis is not simply limited to the maintenance of mitochondrial integrity. A recent study demonstrates that the NatA complex, a protein N- -acetyltransferase complex, is required for DNA damage-mediated apoptosis and suggests that regulation of protein acetylation might provide an important mechanism for regulating apoptotic sensitivity. Since acetyl-CoA (coenzyme A) is a key cofactor for the NatA complex, protein acetylation is subject to the availability of acetyl-CoA and, thus, under metabolic regulation. The revelation that protein N- -acetylation is regulated by Bcl-xL, a major antiapoptotic mitochondrial protein, demonstrates a mechanism by which metabolism can regulate the activation of multiple key apoptotic factors simultaneously.
File Format	HTM / HTML
ISSN	00917451
e-ISSN	19434456
Journal	Cold Spring Harbor Symposia on Quantitative Biology
Volume Number	76
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2011-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biology Apoptosis Cells Cytology Metabolism Animals Apoptosis Regulatory Proteins Models, Biological Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology

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