• Interaction

    AccNo. 55518 Score 0.49
    Name PM_9730893
    Kd 1.0

    Peptide

    AccNo. 55396
    Name YVAD
    Sequence YVAD
    55396_small
    Internalized no
    Is Motif no

    Interactor

    AccNo. 55018
    Name unknown

    Experiment

    AccNo. 55360
    Classification incorrect?
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    Voting_motivation
    CA CVD DM APO ANG MI BD
    0.71 0.59 0.22 0.80 0.43 0.24 0.24 Vote
    plus plus plus plus plus plus plus Yes
    minus minus minus minus minus minus minus No
    Name PM_9730893
    Detection unspecified method, MI:0686
    Source Pubmed Text Id 9730893
    Journal J Exp Med. 1998 Sep 7;188(5):919-30.
    Title Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways.
    Authors Vercammen D, Brouckaert G, Denecker G, Van de Craen M, Declercq W, Fiers W, Vandenabeele P
    Text Murine L929 fibrosarcoma cells were transfected with the human Fas (APO-1/CD95) receptor, and the role of various caspases in Fas-mediated cell death was assessed. Proteolytic activation of procaspase-3 and -7 was shown by Western analysis. Acetyl-Tyr-Val-Ala-Asp-chloromethylketone and benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone++ +, tetrapeptide inhibitors of caspase-1- and caspase-3-like proteases, respectively, failed to block Fas-induced apoptosis. Unexpectedly, the broad-spectrum caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone and benzyloxycarbonyl-Asp(OMe)-fluoromethylketone rendered the cells even more sensitive to Fas-mediated cell death, as measured after 18 h incubation. However, when the process was followed microscopically, it became clear that anti-Fas-induced apoptosis of Fas-transfected L929 cells was blocked during the first 3 h, and subsequently the cells died by necrosis. As in tumor necrosis factor (TNF)-induced necrosis, Fas treatment led to accumulation of reactive oxygen radicals, and Fas-mediated necrosis was inhibited by the oxygen radical scavenger butylated hydroxyanisole. However, in contrast to TNF, anti-Fas did not activate the nuclear factor kappaB under these necrotic conditions. These results demonstrate the existence of two different pathways originating from the Fas receptor, one rapidly leading to apoptosis, and, if this apoptotic pathway is blocked by caspase inhibitors, a second directing the cells to necrosis and involving oxygen radical production.
    Mesh Terms Amino Acid Chloromethyl Ketones/pharmacology; Animals; Antigens, CD95/physiology; Apoptosis/drug effects; Apoptosis/immunology; Caspase 3; Caspase 7; Caspases; Cell Death/drug effects; Cysteine Endopeptidases/metabolism; Cysteine Proteinase Inhibitors/pharmacology; Enzyme Activation/immunology; Fibrosarcoma; Humans; Ligands; Mice; NF-kappa B/metabolism; Necrosis; Oligopeptides/pharmacology; Receptors, Tumor Necrosis Factor/physiology; Signal Transduction/immunology; Transfection/immunology; Tumor Cells, Cultured
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