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FAS — POLDIP2

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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
de la Monte et al., J Alzheimers Dis 2000 : H2O2-treatment resulted in dose dependent increases in cell death due to genomic and mitochondrial DNA damage associated with increased levels of 8-OHdG and the p53 and CD95 pro-apoptosis genes, reduced levels of the Bcl-2 survival gene, activation of JNK and p38 stress kinases, and inhibition of PI3 kinase survival signaling
Galvan et al., J Biol Chem 2003 : Apoptosis signal regulating kinase 1 ( ASK1 ) is a MAP kinase kinase kinase ( MAPKKK ) that is required for c-Jun N-terminal kinase (JNK) and p38 activation in response to Fas and tumor necrosis factor (TNF) receptor stimulation, and for oxidative stress- and TNFalpha induced apoptosis
Starace et al., FASEB J 2005 : By using specific inhibitors for each MAPK, we confirmed the pivotal role of the IkappaB/NF-kappaB system by demonstrating that ERKs, p38 , and JNK are not involved in Fas up-regulation by TNF-alpha
Chen et al., J Cell Biochem 2009 (Calcium Signaling...) : Unlike PLA(2), catalytically inactive PLA(2) treatment did not markedly increase Fas and FasL protein expression, and p38 MAPK activation was exclusively responsible for catalytically inactive PLA(2) induced increase in Fas and 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
Kavuri et al., J Biol Chem 2011 : Analyzing non-apoptotic signaling pathways, we found that TRAIL and CD95L activate JNK and p38 within 15 min. cFLIP variants and different caspase inhibitors blocked late death ligand induced JNK or p38 MAPK activation suggesting that these responses are secondary to cell death
Juo et al., Mol Cell Biol 1997 : In this study, crmA antagonized, and YVAD-CMK and Z-VAD-FMK completely inhibited, Fas activation of p38 kinase activity, demonstrating that Fas dependent activation of p38 requires ICE/CED-3 family members and conversely that the MKK3/p38 activation cascade represents a downstream target for the ICE/CED-3 family proteases
Yue et al., J Biol Chem 1999 : TL1 up-regulated Fas expression in BPAEC at 8 and 24 h after treatment, and significantly activated stress activated protein kinase ( SAPK ) and p38 mitogen activated protein kinase ( p38 MAPK )