Fas ligand

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Related to FASL: Fas protein, Fas receptor

Fas ligand

a molecule on the surface of cytotoxic T cells that binds to its receptor, Fas, on the surface of other cells, initiating apoptosis in the target cell.

Fas li·gand

(fas lī'gand)
A molecule on the surface of cytotoxic T cells that binds to its receptor, Fas, on the surface of other cells, initiating apoptosis in the target cell.
See also: Fas

fas ligand

Abbreviation: FasL
A protein on the surface of activated T cells that binds to Fas receptors on the surface of the same or other T cells and triggers a series of events causing apoptosis. This process is involved in the activation-induced cell death necessary to ensure that autoreactive T cells do not attack “self” antigens.
See also: ligand
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The presented data strongly support the idea that AREG reduces extrinsic apoptosis in neonatal monocytes via gelatinase-induced FasL cleavage.
There were no statistically significant differences between the expression of gastric cancer cell proteins: FHIT, p-catenin, y-catenin, cathepsin B, EGF, HER-2, MMP-9, MCM-2, Bak, Bax, BclXL, p53, FasL and Procaspase 3, depending on the classification according to Lauren (Table 2).
Interaction of Fas- FasL or TNFa molecules could be the signal to the development of apoptosis.
sFas plays a role as an antiapoptotic molecule that blocks FasL or sFasL binding, and its concentration in the serum of healthy subjects is independent of gender and age [23].
When the stochastic weather simulator was added, the model simulated historic sea elevations reasonably well with a difference of only 1 foot at its most disparate point, -228 fasl (simulated) and -229 fasl (historic), and maintained patterns of seasonality.
Aside from the tumor necrosis factor (TNF) and the Fas ligand (FasL), the TNF-related apoptosis-inducing ligand (TRAIL), also known as the apoptosis 2 ligand or Apo2L (1), is a member of the TNF superfamily that induces apoptosis by binding to specific death receptors and activating multiple apoptotic signaling pathways (2).
Skin from aged participants (n = 14; mean 70.7 years), and young participants (n = 14; mean 23.4 years) was grafted to beige SCID mice, and epidermal thickness, proliferation (Ki-67 expression), apoptosis (TUNEL [Tdt-mediated dUTP nick end labeling] reaction below granular layer), and expression of Fas and FasL were determined by histology and immunochemical staining.
Conversely, alternatively activated M2-type macrophages do not secrete the proinflammatory mediators IL-1B or TNF-[alpha] [32] and are believed to exert immunomodulation primarily through secretion of the potent immunosuppressive cytokines IL-10, IL-6, and TGF-[beta], downregulation of cell surface molecules necessary for antigen presentation including MHC II, CD80, and CD86, decreased phagocytic capacity, and upregulation of cell surface antigens FasL and B7-H1 both known to stimulate programmed cell death in lymphocytes, among other effects [29, 33, 34].
Another mechanism by which endometriotic cells are able to escape from immune surveillance of cytotoxic T lymphocyte is attributable to FasL expressed by endometriotic cells.