◀ Back to EPHB2

EPHB2 — 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
Choi et al., Cancer Res 2001 (Glioblastoma...) : Herein, we demonstrate that : ( a ) stimulation with agonistic anti-Fas monoclonal antibody CH-11 and human recombinant soluble Fas ligand induces expression of the CC chemokine MCP-1 and the CXC chemokine interleukin-8 by human glioma cell lines at the mRNA and protein levels in a dose- and time dependent manner ; ( b ) selective pharmacological inhibitors of MEK1 ( U0126 and PD98059 ) and p38 mitogen activated protein kinase ( MAPK ) ( SB202190 ) suppress Fas mediated chemokine expression in a dose dependent manner ; ( c ) Fas ligation on human glioma cells leads to activation of both extracellular signal regulated kinases ERK1/ERK2 and p38 MAPK ; and ( d ) GBM samples express higher levels of Fas compared with normal control brain, which correlates with increased interleukin 8 expression
Scheller et al., Eur J Immunol 2002 (Inflammation...) : Further analysis with A3.01 T cells revealed that the proinflammatory signaling activity of CD95 was mediated by MEK/ERK , p38 and NF-kappaB signaling pathways
Desbarats et al., Nat Cell Biol 2003 : Fas engagement induces neurite growth through ERK activation and p35 upregulation
Ceccatelli et al., Toxicol Lett 2004 : The Fas induced ERK phosphorylation that we detect in C17.2 cells suggests that in NSC Fas may function as a mediator of growth rather than death
Kogianni et al., Life Sci 2004 : ERK activation by PMA did not induce death or Fas upregulation, suggesting that Fas may be important for the induction of apoptosis and the existence of an additional factor activated by Dex which enables the cooperation between the Dex activated ERK and Fas pathways, during apoptosis of osteocytes
Iordanov et al., J Invest Dermatol 2005 (Dermatitis) : Using a variety of inhibitors and blocking antibodies, we demonstrated that : ( i ) apoptosis is required for the generation of the signal ( s ) leading to the activation of EGFR, ERK, and Akt; (ii) the activation of EGFR, ERK , and Akt by FasL is indeed mediated by its bona fide receptor Fas ; ( iii ) the activation of EGFR is essential for the subsequent activation of ERK and Akt ; and ( iv ) apoptotic keratinocytes secrete soluble EGFR ligands ( including amphiregulin ) that are processed from membrane bound proligand forms by metalloproteinase ( s )
Lee et al., EMBO J 2006 : In contrast, CD95 ligand stimulation of cells unable to internalize CD95 results in activation of proliferative Erk and NF-kappaB signaling pathways
Cagnol et al., Apoptosis 2006 : Accordingly, prolonged ERK stimulation activated caspase 8 and strongly potentiated Fas signaling
Reinehr et al., Gastroenterology 2008 (Disease Models, Animal...) : CD95L induced EGFR and Erk phosphorylation were abolished after proteinase inhibition by GM6001 and in the presence of neutralizing epidermal growth factor antibodies, suggestive of a ligand dependent EGFR phosphorylation in response to CD95L
Liu et al., J Cell Physiol 2009 (MAP Kinase Signaling System) : Activated ERK suppressed p38 MAPK activation and Fas/FasL protein expression
Shin et al., Int J Hematol 2010 : To distinguish between the activation signalling and the death inducing pathway downstream of Fas, we generated a novel T cell line expressing a chimeric hCD8-FasC protein and found that stimulation with the anti-CD8 antibodies induced tyrosine phosphorylation of TCR-proximal proteins, activation of Raf-1/ERK , p38 and JNK, and increased expression of CD69, Fas , and Fas ligand
Yuan et al., J Biol Chem 2011 (MAP Kinase Signaling System...) : Furthermore, increased phosphorylation of Src was demonstrated to mediate Fas induced ERK activation and cell survival
Rapold et al., J Lipid Res 2013 : In parallel, Fas activation increased phosphorylation of ERK1/2 , and FasL induced lipolysis was blunted in the presence of the ERK-inhibitor U0126 or in ERK1/2 depleted adipocytes
Su et al., Cell Immunol 2013 : Although the ligation of Fas results in caspase-8 cleavage and ERK1/2 phosphorylation, inhibitors for caspase-8 and MEK have no effect on the expressions of ROR?t, IL-17A, and IL-17F