◀ Back to FAS

ASIP — FAS

Text-mined interactions from Literome

Shinohara et al., Cancer Res 2000 (Glioma...) : We report here that : ( a ) in gliomas, [ 3H ] TdR incorporation was enhanced by anti-Fas IgM monoclonal antibody CH-11 and conversely inhibited by anti-FasL monoclonal antibody NOK-2 ; ( b ) cross linking of Fas with CH-11 drove both cell cycle progression and apoptosis as demonstrated by the induction of the S-G2 phase of DNA and RNA and fragmented nuclei ; ( c ) phosphorylation of extracellular signal regulated kinase ( ERK ), but not of c-Jun NH2-terminal kinase or p38, was induced by cross linking of Fas ; ( d ) a mitogen activated protein kinase/ERK kinase 1 ( MEK1 ) inhibitor PD98059 completely blocked CH-11 induced ERK phosphorylation as well as cell cycle progression without affecting induction of apoptosis ; and ( e ) a broad-spectrum caspase inhibitor Z-Asp-CH2-DCB inhibited CH-11 induced ERK phosphorylation, cell cycle progression, and apoptosis
Lens et al., J Immunol 1998 : The caspase inhibitor Val-Ala-Asp-fluoromethylketone blocked both Fas- and BCR mediated apoptosis, but differentially affected caspase 3 cleavage induced by either stimulus