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ARSK — CASP7

Text-mined interactions from Literome

Hatai et al., J Biol Chem 2000 : Consistently, caspase-8-deficient ( Casp8 ( -/- ) ) cells were sensitive to ASK1 induced caspase-3 activation and apoptosis, suggesting that caspase-8 is dispensable for ASK1 induced apoptosis, whereas ASK1 failed to activate caspase-3 in caspase-9-dificient ( Casp9 ( -/- ) ) cells
Liu et al., Circ Res 2002 : Finally, we showed that the single mutants ( not Trx-WT ) significantly ( n=4 and P < 0.05 ) inhibited ASK1 induced JNK activation, caspase 3 activity, and apoptosis in TNF/ROS-resistant manner
Bhattacharyya et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Of foremost interest in the present study was the finding that ASK1/p38 signaling was essential for caspase 8 activation linked to M. avium induced death signaling
Kutuzov et al., J Biol Chem 2005 : In line with the decreased ASK1 activation, polyamine depletion in COS-7 cells abrogated oxidative stress induced activation of caspase-3, which executes ASK1 induced apoptosis, as well as caspase-3 activation induced by ASK1 overexpression, but had no effect on basal caspase-3 activity
Cataldi et al., J Mol Histol 2005 (Anoxia...) : In contrast, ASK-1 mediated JNK/SAPK activation, regulating Bcl(2) levels, allows Bax homodimerization and caspase-3 activation in the same experimental conditions
Shi et al., FEBS Lett 2011 : HG induced activation of apoptosis signal regulating kinase-1 ( ASK1 ) in a time dependent manner in MMCs. Treatment with antioxidant, tempol, or knockdown of TXNIP in MMCs reduced HG-mediated apoptosis, expression of cleaved caspase-3 , Bax/Bcl-2 ratio and activation of ASK1
Chen et al., Oncogene 1999 : Overexpression of kinase negative ASK1 ( K709R ), which inhibited ASK1 activation and the downstream MKK3-p38 and MKK4-JNK1 pathways, also suppressed the caspase protease activation and apoptosis induced by cDDP