PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Arsenic Trioxide 13-18 caspase 8 Homo sapiens 94-103 25815518-9 2015 VPA and ATO had synergistic effects on the proliferation of RPMI8226 cells, which may have been associated with the decreased expression of Bcl-2 and the increased expression levels of Bcl-2-associated X protein, Caspase 8 and Caspase 9. Arsenic Trioxide 8-11 caspase 8 Homo sapiens 213-222 24627159-7 2014 We also confirmed the anti-NF-kappaB activity of As4O6 with synergism with TNF-alpha by augmenting caspase-8 activation. Arsenic Trioxide 49-54 caspase 8 Homo sapiens 99-108 25130820-9 2014 It is concluded that VPA can enhance the sensitivity of RPMI 8226 cells to ATO-induced apoptosis, which may be associated with decreasing the BCL-2 expression and increasing the BAX, caspase-8 and caspase-9 gene expression. Arsenic Trioxide 75-78 caspase 8 Homo sapiens 183-192 16434995-0 2006 TRAIL sensitisation by arsenic trioxide is caspase-8 dependent and involves modulation of death receptor components and Akt. Arsenic Trioxide 23-39 caspase 8 Homo sapiens 43-52 20953137-7 2010 ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells. Arsenic Trioxide 0-3 caspase 8 Homo sapiens 110-119 20953137-8 2010 ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells. Arsenic Trioxide 0-3 caspase 8 Homo sapiens 19-27 18566239-8 2008 We show that As2O3 decreases AKT protein via caspase-mediated degradation, abrogated by caspase-6, caspase-8, caspase-9, and caspase-3 inhibitors but not proteosome inhibitors. Arsenic Trioxide 13-18 caspase 8 Homo sapiens 99-108 18359480-3 2008 Co-treatment with ATO plus quercetin caused mitochondrial transmembrane potential dissipation, stimulated the mitochondrial apoptotic pathway, as indicated by cytochrome c and Omi/Htra2 release, XIAP and Bcl-X(L) down-regulation, and Bax activation, and caused caspase-8/Bid activation. Arsenic Trioxide 18-21 caspase 8 Homo sapiens 261-270 18173754-6 2008 The increase of apoptosis by the combination of ATO and SB203580 was accompanied by the activation of caspase-9 and caspase-8 suggesting that both extrinsic and intrinsic apoptotic pathways are involved. Arsenic Trioxide 48-51 caspase 8 Homo sapiens 116-125 17145888-6 2006 Treatment with As(2)O(3) plus BSO, but not with As(2)O(3) alone, increased the levels of death receptor (DR) 5 protein and caspase-8 cleavage. Arsenic Trioxide 15-24 caspase 8 Homo sapiens 123-132 16685442-0 2006 Combination treatment with arsenic trioxide and sulindac augments their apoptotic potential in lung cancer cells through activation of caspase cascade and mitochondrial dysfunction. Arsenic Trioxide 27-43 caspase 8 Homo sapiens 135-142 21779797-0 2012 Arsenic trioxide induces human pulmonary fibroblast cell death via the regulation of Bcl-2 family and caspase-8. Arsenic Trioxide 0-16 caspase 8 Homo sapiens 102-111 21779797-10 2012 In conclusion, HPF cells were resistant to ATO and higher doses of ATO induced the growth inhibition and death in HPF cells via the regulation of Bcl-2 family and caspase-8. Arsenic Trioxide 67-70 caspase 8 Homo sapiens 163-172 17673311-7 2007 P38-MAPK-specific inhibitors attenuate the As(2)O(3) plus TNFalpha-provoked activation of caspase-8/Bid, Bax translocation, cytochrome c release, and apoptosis induction. Arsenic Trioxide 43-52 caspase 8 Homo sapiens 90-99 16434995-3 2006 The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex. Arsenic Trioxide 19-22 caspase 8 Homo sapiens 70-79 16434995-3 2006 The combination of ATO and TRAIL synergistically enhanced cleavage of caspase-8, which was blocked by the caspase inhibitor IETD.fmk as well as in cells deficient for caspase-8, suggesting a requirement for the death-inducing signalling complex. Arsenic Trioxide 19-22 caspase 8 Homo sapiens 167-176 12851490-0 2003 Arsenic trioxide selectively induces early and extensive apoptosis via the APO2/caspase-8 pathway engaging the mitochondrial pathway in myeloma cells with mutant p53. Arsenic Trioxide 0-16 caspase 8 Homo sapiens 80-89 14726646-5 2004 ATO rapidly induced Apo2/TRAIL, activation of caspase 8, cleavage of BID, depolarization of mitochondrial membrane (MM) and release of AIF from mitochondria in a Bcl-2 independent fashion. Arsenic Trioxide 0-3 caspase 8 Homo sapiens 46-55 16007134-3 2005 Here, we address a potential role of death receptor signaling through the FADD/caspase-8 death-inducing signaling complex in As2O3-induced cell death. Arsenic Trioxide 125-130 caspase 8 Homo sapiens 79-88 16010437-5 2005 ATO activated the intrinsic (mitochondrial) pathway of apoptosis, which involved disrupting mitochondrial membrane potential, increased Bax/Bcl-2 ratio and caspase-9 activation, as well as the extrinsic (death receptor) pathway mediated by Fas and caspase-8 activation. Arsenic Trioxide 0-3 caspase 8 Homo sapiens 248-257 12851490-3 2003 In cells expressing mutated p53, ATO induced, G2/M arrest and activation caspase 8 and 3 and rapid and extensive apoptosis. Arsenic Trioxide 33-36 caspase 8 Homo sapiens 73-88 12684647-5 2003 As2O3-treated cell lines also showed upregulation of CD95/CD95L expression and activation of caspases 8 and 3. Arsenic Trioxide 0-5 caspase 8 Homo sapiens 93-109 12531793-0 2003 Arsenic trioxide-induced apoptosis in myeloma cells: p53-dependent G1 or G2/M cell cycle arrest, activation of caspase-8 or caspase-9, and synergy with APO2/TRAIL. Arsenic Trioxide 0-16 caspase 8 Homo sapiens 111-120 12531793-6 2003 The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53. Arsenic Trioxide 181-184 caspase 8 Homo sapiens 161-177 11021749-0 2000 Involvement of CD95-independent caspase 8 activation in arsenic trioxide-induced apoptosis. Arsenic Trioxide 56-72 caspase 8 Homo sapiens 32-41 11866444-2 2002 HLE cells underwent apoptosis at 2 microM ATO, which was executed by the activation of caspase-3 through the mitochondrial pathway mediated by caspase-8 activation and Bid truncation. Arsenic Trioxide 42-45 caspase 8 Homo sapiens 143-152 11021749-7 2000 Caspase 8 and Bid were also activated by As2O3 in NB4 but not in NB4/As. Arsenic Trioxide 41-46 caspase 8 Homo sapiens 0-9 11021749-14 2000 These findings suggest that the As2O3 treatment activates caspase 8 in a CD95-independent but GSH concentration-dependent manner. Arsenic Trioxide 32-37 caspase 8 Homo sapiens 58-67