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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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Journal ArticleDOI

A family of transmembrane proteins with homology to the MET-hepatocyte growth factor receptor

TL;DR: In this paper, a transmembrane protein (SEX) of 1871 amino acids was identified on Xq28 encoding a highly conserved sequence, which shares significant homology with the extracellular domain of the receptors encoded by the oncogenes MET, RON, and SEA [hepatocyte growth factor (HGF) receptor family].
Journal ArticleDOI

Fas/Fas Ligand Interaction Contributes to UV-Induced Apoptosis in Human Keratinocytes

TL;DR: The data strongly suggest that the Fas system contributes to keratinocyte apoptosis in UV-irradiated human skin.
Journal ArticleDOI

Regulation mechanism of selective atresia in porcine follicles: regulation of granulosa cell apoptosis during atresia.

TL;DR: It is shown that the porcine granulosa cell is a type II apoptotic cell, which has the mitochondrion-dependent apoptosis-signaling pathway, and the cell death receptor-mediated apoptosis signaling pathway ingranulosa cells has been suggested to be as follows.
Journal Article

The Fas-Fas ligand system and other modulators of apoptosis in the cornea.

TL;DR: The Fas system (Fas and Fas ligand) modulators and final common pathway mediators of apoptosis are expressed in corneal cells and the Fas-Fas ligand system is expressed in the cornea and could have important functions in normal cornea physiology and in the pathophysiology of cornea disease, including modulation of keratocyte apoptosis after epithelial injury.
References
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Journal ArticleDOI

Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis

TL;DR: The Ipr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus.
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The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis.

TL;DR: Complementary DNAs encoding the cell surface antigen Fas were isolated from a cDNA library of human T cell lymphoma KT-3 cells and revealed that the molecule coding for the Fas antigen determinant is a 319 amino acid polypeptide with a single transmembrane domain.
Journal ArticleDOI

Social controls on cell survival and cell death

TL;DR: For some mammalian cells, programmed death seems to occur by default unless suppressed by signals from other cells, so dependence on specific survival signals provides a simple way to eliminate misplaced cells, for regulating cell numbers and, perhaps, for selecting the fittest cells.
Journal ArticleDOI

Molecular cloning and expression of the fas ligand, a novel member of the tumor necrosis factor family

TL;DR: Northern hybridization revealed that Fas ligand is expressed in activated splenocytes and thymocytes, consistent with its involvement in T cell-mediated cytotoxicity and in several nonlymphoid tissues, such as testis.
Journal ArticleDOI

Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes.

TL;DR: The CD8+ effector cells raised in the CD4 subset- deficient host were able of clear vital tissues from productive infection and to restrict asymptomatic, persistent infection to acinar glandular epithelial cells in salivary gland tissue.
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