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Fas‐induced apoptosis, and diseases caused by its abnormality
Author(s) -
Nagata Shigekazu
Publication year - 1996
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.1996.d01-214.x
Subject(s) - fas ligand , biology , apoptosis , microbiology and biotechnology , fas receptor , programmed cell death , cytotoxic t cell , immunology , genetics , in vitro
Homeostasis of multicellular organisms is controlled not only by proliferation and differentiation of cells but also by cell death. Physiological cell death mostly proceeds by apoptosis, a process which includes condensation and segmentation of the nuclei and cytoplasm, and often extensive fragmentation of chromosomal DNA into nucleosome units. Molecular and cellular characterization of Fas, a cell‐surface protein recognized by cytotoxic monoclonal antibodies, has led to its definition as a receptor for a Fas ligand (FasL). FasL binds to Fas, which results in target cell apoptosis. A family of cysteine proteases seems to be sequentially activated during the Fas‐mediated apoptosis. The phenotypes of the loss‐of‐function mutants of Fas and FasL indicate that this system is involved in T cell‐mediated cytotoxicity, in down‐regulation of immune responses, and probably in the turnover of senescent cells. Malfunction of the Fas system causes hyperplasia in peripheral lymphoid organs and the liver, accelerating autoimmune diseases and tumorigenesis, whereas exaggeration of the system leads to tissue disruption.