PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11709711-0 2001 Protein kinase C inhibits singlet oxygen-induced apoptosis by decreasing caspase-8 activation. Singlet Oxygen 26-40 caspase 8 Homo sapiens 73-82 11709711-2 2001 We have shown previously that caspase-8 and p38 mediate singlet oxygen-induced apoptosis in HL-60 cells. Singlet Oxygen 56-70 caspase 8 Homo sapiens 30-39 11709711-3 2001 In this study, we investigated the influence of PKC on regulation of the caspase and p38 pathways initiated by singlet oxygen. Singlet Oxygen 111-125 caspase 8 Homo sapiens 73-80 11709711-4 2001 Singlet oxygen induced Fas clustering and subsequent recruitment of FADD and caspase-8. Singlet Oxygen 0-14 caspase 8 Homo sapiens 77-86 11709711-6 2001 Surprisingly, under the same conditions PKC activation was still able to prevent singlet oxygen-induced activation of caspase-8 and block its downstream signaling events including cleavage of Bid and caspase-3, decrease in mitochondrial transmembrane potential and release of cytochrome c from mitochondria. Singlet Oxygen 81-95 caspase 8 Homo sapiens 118-127 11709711-9 2001 These data indicate that PKC inhibits singlet oxygen-induced apoptosis by blocking activation of caspase-8. Singlet Oxygen 38-52 caspase 8 Homo sapiens 97-106 10837470-6 2000 In contrast, blockade of caspase-8 with Ile-Glu-Thr-Asp-fluoromethyl ketone is sufficient to prevent formation of DNA fragments and to inhibit all the above signaling events, with exception of p38 phosphorylation, in both singlet oxygen- and H(2)O(2)-treated cells. Singlet Oxygen 222-236 caspase 8 Homo sapiens 25-34 10837470-7 2000 These data suggest that caspase-3 activation is regulated through redundant signaling pathways that involve p38 and caspase-8 acting upstream of Bid during singlet oxygen-induced apoptosis, whereas the activation of caspase-3 by H(2)O(2) is only governed by a caspase-8-mediated apoptotic pathway. Singlet Oxygen 156-170 caspase 8 Homo sapiens 116-125 10837470-7 2000 These data suggest that caspase-3 activation is regulated through redundant signaling pathways that involve p38 and caspase-8 acting upstream of Bid during singlet oxygen-induced apoptosis, whereas the activation of caspase-3 by H(2)O(2) is only governed by a caspase-8-mediated apoptotic pathway. Singlet Oxygen 156-170 caspase 8 Homo sapiens 260-269 26225731-8 2015 It depended on singlet oxygen-dependent activation of the FAS receptor and caspase-8, followed by caspase-8-mediated enhancement of NOX activity. Singlet Oxygen 15-29 caspase 8 Homo sapiens 75-84 10388534-0 1999 Caspase-8 mediates caspase-3 activation and cytochrome c release during singlet oxygen-induced apoptosis of HL-60 cells. Singlet Oxygen 72-86 caspase 8 Homo sapiens 0-9 10388534-5 1999 Further studies showed that singlet oxygen induced an increase in caspase-8 activity and a reduction in mitochondrial cytochrome c. Singlet Oxygen 28-42 caspase 8 Homo sapiens 66-75 10388534-8 1999 These results suggest that caspase-8 mediates caspase-3 activation and cytochrome c release during singlet oxygen-induced apoptosis in HL-60 cells. Singlet Oxygen 99-113 caspase 8 Homo sapiens 27-36 25619142-6 2015 Singlet-oxygen-dependent activation of the FAS receptor and caspase-8 increased superoxide anion generation by NOX1 and amplification of singlet oxygen generation, which allowed singlet-oxygen-dependent inactivation of catalase. Singlet Oxygen 137-151 caspase 8 Homo sapiens 60-69 25653236-9 2015 This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase. Singlet Oxygen 43-57 caspase 8 Homo sapiens 139-147 25653236-9 2015 This allows the formation of extracellular singlet oxygen through the reaction between H(2)O(2) and peroxynitrite, amplification through a caspase8-dependent step and subsequent singlet oxygen-mediated inactivation of catalase. Singlet Oxygen 178-192 caspase 8 Homo sapiens 139-147