Apoptosis signaling
Journal Title
ANNUAL REVIEW OF BIOCHEMISTRY
Publication Type
Journal Article
Abstract
Apoptosis, a physiological process for killing cells, is critical for the normal development and function of multicellular organisms. Abnormalities in cell death control can contribute to a variety of diseases, including cancer, autoimmunity, and degenerative disorders. Signaling for apoptosis occurs through multiple independent pathways that are initiated either from triggering events within the cell or from outside the cell, for instance, by ligation of death receptors. All apoptosis signaling pathways converge on a common machinery of cell destruction that is activated by a family of cysteine proteases (caspases) that cleave proteins at aspartate residues. Dismantling and removal of doomed cells is accomplished by proteolysis of vital cellular constituents, DNA degradation, and phagocytosis by neighboring cells. This article reviews current knowledge of apoptosis signaling, lists several pressing questions, and presents a novel model to explain the biochemical and functional interactions between components of the cell death regulatory machinery.
Publisher
ANNUAL REVIEWS
Keywords
PROGRAMMED CELL-DEATH; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; DOMAIN-CONTAINING RECEPTOR; BCL-X-L; INTERLEUKIN-1-BETA CONVERTING-ENZYME; FACTOR RECEPTOR-1-INDUCED APOPTOSIS; SURVIVAL-PROMOTING PROTEINS; FADD-DEPENDENT APOPTOSIS; INHIBITS MULTIPLE FORMS
Rights Notice
Refer to copyright notice on published article.


Creation Date: 2000-01-01 12:00:00
Last Modified: 0001-01-01 12:00:00
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