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Journal ArticleDOI

The Fas Death Factor

Shigekazu Nagata, +1 more
- 10 Mar 1995 - 
- Vol. 267, Iss: 5203, pp 1449-1456
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TLDR
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells.
Abstract
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells. Various cells express Fas, whereas FasL is expressed predominantly in activated T cells. In the immune system, Fas and FasL are involved in down-regulation of immune reactions as well as in T cell-mediated cytotoxicity. Malfunction of the Fas system causes lymphoproliferative disorders and accelerates autoimmune diseases, whereas its exacerbation may cause tissue destruction.

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Citations
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Journal ArticleDOI

Apoptosis by death factor.

TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
Journal ArticleDOI

Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion

TL;DR: It is reported here that, except for cells of the macrophage lineage, normal human tissues do not express B7-H1 and the findings have implications for the design of T cell–based cancer immunotherapy.
Journal ArticleDOI

The TNF and TNF receptor superfamilies: integrating mammalian biology.

TL;DR: The authors regret the inability to cite all of the primary literature contributing to this review due to length considerations, but wish to thank F. Chan, T. Migone, and J. Wang for insightful comments on the manuscript.
Journal ArticleDOI

A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD

TL;DR: A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells and seems to function as a chaperone for CAD during its synthesis, remaining complexed with CAD to inhibit its DNase activity.
Journal ArticleDOI

FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.

TL;DR: This work utilized nano-electrospray tandem mass spectrometry to identify CAP3 and CAP4, components of the CD95 (Fas/APO-1) death-inducing signaling complex, and found a novel 55 kDa protein, designated FLICE, which has homology to both FADD and the ICE/CED-3 family of cysteine proteases.
References
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Journal ArticleDOI

Fas and Fas ligand: lpr and gld mutations

TL;DR: The physiological role of the Fas system in T-cell development, cytotoxicity and cytotoxic T lymphocyte (CTL)-mediated autoimmune disease is discussed and current knowledge of Fas and FasL is summarized.
Journal ArticleDOI

Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen.

TL;DR: The APO-1 antigen was expressed upon transfection of APo-1 cDNA into BL60-P7 Burkitt's lymphoma cells and conferred sensitivity towards anti-APO- 1-induced apoptosis to the transfectants.
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Extrathymic tolerance of mature T cells: clonal elimination as a consequence of immunity.

TL;DR: Evidence is presented that exposure of mature T cells to Mlsa antigens in vivo leads to specific tolerance and disappearance of MlsA-reactive V beta 6+ T cells, raising important questions concerning the relationship of tolerance and memory.
Journal ArticleDOI

Cloning and functional analysis of BAG-1: A novel Bcl-2-binding protein with anti-cell death activity

TL;DR: The findings indicate that bag-1 represents a new type of anti-cell death gene and suggest that some routes of apoptosis induction previously ascribed to Bcl-2-independent pathways may instead reflect a need for the combination of B cl-2 and BAG-1.
Journal ArticleDOI

Cytotoxic lymphocytes require granzyme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cells

TL;DR: It is concluded that gzm B serves a critical and nonredundant role for the rapid induction of target cell DNA fragmentation and apoptosis by alloreactive cytotoxic T lymphocytes.
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