PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18569012-3 2008 25-OH-chol increased the production of reactive oxygen species and opened mitochondrial permeability transition pore, resulting in release of cytochrome c and subsequent activation of caspase-9 and -3. Reactive Oxygen Species 39-62 caspase 9 Rattus norvegicus 184-200 22166790-4 2012 In addition, I6-induced reactive oxygen species (ROS) caused the disruption of mitochondria membrane potential (MMP), the release of cytochrome c, the activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP), resulting in activation of mitochondrial-mediated intrinsic death pathway. Reactive Oxygen Species 24-47 caspase 9 Rattus norvegicus 165-174 22166790-4 2012 In addition, I6-induced reactive oxygen species (ROS) caused the disruption of mitochondria membrane potential (MMP), the release of cytochrome c, the activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP), resulting in activation of mitochondrial-mediated intrinsic death pathway. Reactive Oxygen Species 49-52 caspase 9 Rattus norvegicus 165-174 16514665-9 2006 The results showed that Hcy-mediated ROS production preceded the loss of MP, the release of cytochrome-c, and the activation of caspase-9 and -3. Reactive Oxygen Species 37-40 caspase 9 Rattus norvegicus 128-144 16514665-14 2006 Our data suggested that Hcy-mediated ROS production promotes endothelial cell death in part by disturbing MP, which results in subsequent release of cytochrome-c and activation of caspase-9 and 3, leading to cell death. Reactive Oxygen Species 37-40 caspase 9 Rattus norvegicus 180-195 15135649-9 2004 These results suggest that BR931 can increase generation of ROS, leading to DNA damage and p53 phosphorylation, which, in turn, induces the activation of Bax, release of cytochrome-c from mitochondria and activation of caspases, culminating in cell death. Reactive Oxygen Species 60-63 caspase 9 Rattus norvegicus 219-227