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BCL10 — FAS

Text-mined interactions from Literome

Almawi et al., J Leukoc Biol 2004 : The antagonism of apoptosis afforded by prosurvival Bcl-2 proteins appeared to be specific for the GCs, as Bcl-2 and Bcl-x ( L ) blocked GC-induced apoptosis in T cell hybridomas but did not affect Fas or activation induced apoptosis
Wu et al., Environ Toxicol 2013 : Western blot analysis demonstrated that propofol promoted Fas , cytochrome c, caspase-9 and -3 active form and Bax levels, but inhibited Bcl-xl protein level which led to cell apoptosis
Brás et al., J Immunol 1997 (Lymphoma, B-Cell) : In this system, Fas ligation also triggers Bcl-2/Bcl-x down-regulation, an effect inhibited by sIgG cross linking, the cysteine protease inhibitor acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone, and PMA treatment ... In A20 cells, Fas signaling may thus trigger both ICE activation and Bcl-x and Bcl-2 down-regulation
Srinivasan et al., J Biol Chem 1998 (Breast Neoplasms) : Bcl-xL functions downstream of caspase-8 to inhibit Fas- and tumor necrosis factor receptor 1-induced apoptosis of MCF7 breast carcinoma cells ... In some cells, Bcl-xL overexpression can inhibit anti-Fas- and tumor necrosis factor (TNF)-alpha induced apoptosis
Fulda et al., Cancer Res 1998 (Neuroblastoma) : After Doxo treatment, enhanced CD95/CD95-L expression and caspase-8 activation were not blocked by Bcl-2 or Bcl-X ( L ) and were found in cells with a mitochondrial transmembrane potential ( delta psi ( m ) ) that was still normal ( delta psi ( m ) high cells )