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ADAM10 regulates FasL cell surface expression and modulates FasL-induced cytotoxicity and activation-induced cell death [PDF]

open access: yesCell Death and Differentiation, 2007
The apoptosis-inducing Fas ligand (FasL) is a type II transmembrane protein that is involved in the downregulation of immune reactions by activation-induced cell death (AICD) as well as in T cell-mediated cytotoxicity. Proteolytic cleavage leads to the generation of membrane-bound N-terminal fragments and a soluble FasL (sFasL) ectodomain. sFasL can be
Thorsten Maretzky   +2 more
exaly   +3 more sources
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Fas/FasL of pacific cod mediated apoptosis

Developmental & Comparative Immunology, 2021
Fas and Fas ligand (FasL) pathway plays important roles in virus defense and cell apoptosis. In our previous work, nervous necrosis virus (NNV) was discovered in Pacific cod (Gadus macrocephalus), and the Fas ligand (PcFasL) was up-regulated when NNV outbreak, however, signal transmission of Fas/FasL in fish are still unclear.
Ming-Guang, Mao   +5 more
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Fas (CD95)/FasL (CD178) system during ageing

Cell Biology International, 2023
AbstractThe Fas/FasL system plays a central role in the physiological regulation of apoptosis and has been implicated in the pathogenesis of several neoplasms and diseases of the immune system. Until now, it has received little attention in the context of ageing, but there is sufficient evidence that it plays an important role in this process and its ...
openaire   +2 more sources

FasL Expression and Reverse Signalling

2009
FasL plays a central role in the induction of apoptosis within the immune system. It mediates activation-induced cell death (AICD) of T lymphocytes and contributes to the cytotoxic effector function of T and NK cells. Moreover, FasL is discussed as direct effector molecule for the establishment of immune privilege and tumour survival. Besides its death-
M, Lettau   +3 more
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FasL and Fas

2007
The membrane receptor Fas is one of the central members of the TNF receptor superfamily, representing the prototype of an apoptosis inducer. Its cognate ligand, FasL, is expressed as a type II transmembrane protein, but also exists as a soluble molecule.
Anja Krippner-Heidenreich   +1 more
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Differential protein–protein interactions of full length human FasL and FasL fragments generated by proteolysis

Experimental Cell Research, 2014
Fas ligand (FasL) is a death factor of the tumor necrosis factor superfamily. Like other members of this family of type II transmembrane proteins, FasL is subject to ectodomain shedding by a disintegrin and metalloproteinases (ADAMs) liberating soluble FasL and leaving membrane-integral N-terminal fragments (NTFs).
Marcus, Lettau   +4 more
openaire   +2 more sources

FasL, leukocytes and vascular modeling

Nature Medicine, 2004
The recent paper by Ishida et al.1 examines the role of leukocytes, specifically T lymphocytes, in vascular remodeling and vaso-obliteration in the rat eye. The authors conclude that T lymphocytes bind to the vasculature and model it by using Fas ligand (FasL) to prune the developing vessels.
Thomas A Ferguson, Patrick M Stuart
openaire   +1 more source

FasL Binds Preassembled Fas

Science, 2000
The binding of a ligand to its receptor has always been viewed as the trigger for signal transduction to ensue. However, as [Golstein][1] explains in his Perspective, new findings ([ Chan et al .][2] and [ Siegel et al .][3]) suggest that the Fas receptor preassembles into trimers without the help of its ligand, and that this preassembly conditions ...
openaire   +1 more source

FasL-Independent Activation of Fas

2007
Fas death receptor (also named CD95 or APO-1) is physiologically activated through binding to its cognate ligand, FasL. Fas/FasL interaction induces oligomerization and aggregation of Fas receptor, leading eventually to apoptosis after protein-protein interac­ tions with adaptor and effector proteins.
Faustino Mollinedo, Consuelo Gajate
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Cellular Automata Modeling of FASL‐Initiated Apoptosis

Chemistry & Biodiversity, 2010
AbstractTwo strategies for fighting cancer by modulating FASL‐induced apoptosis were modeled by 2D‐cellular automata. Our models predict that cancer cells can be killed by maximizing the apoptosis via joint suppression of FLIP and IAP inhibitors by siRNA and SMAC proteins, respectively. It was also predicted that the presumed feedback loop CASP3→CASP9→|
Advait, Apte   +2 more
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