PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25060904-7 2014 Inhibition of the de novo sphingolipid pathway (myriocin) or GCS (EtPoD4) induced endothelial barrier dysfunction and increased caspase 3-mediated cell death in response to hypoxia. Sphingolipids 26-38 caspase 3 Homo sapiens 128-137 30399362-10 2019 Aberrant sphingolipid homeostasis was associated with reduced cell viability, increased necrosis, procaspase-3 and PARP processing, caspase-3 activity, and decreased AKTS473 phosphorylation. Sphingolipids 9-21 caspase 3 Homo sapiens 98-110 30399362-10 2019 Aberrant sphingolipid homeostasis was associated with reduced cell viability, increased necrosis, procaspase-3 and PARP processing, caspase-3 activity, and decreased AKTS473 phosphorylation. Sphingolipids 9-21 caspase 3 Homo sapiens 101-110 11483620-5 2001 Activation of caspase-3-like enzyme occurred after addition of lysosphingolipids followed by incubation at 37 degrees C for 24 h. The addition of an inhibitor of caspases, ZVAD-fmk, to the Neuro2a cell culture completely inhibited the elevation of caspase-3 activity but not the DNA fragmentation. Sphingolipids 63-80 caspase 3 Homo sapiens 14-23 15596715-5 2004 Myriocin and fumonisin B1, specific inhibitors of key enzymes (serine palmitoyltransferase and dihydroceramide synthase, respectively) in de novo synthesis of sphingolipids, significantly protected cells from gammaT-induced DNA fragmentation, cytochrome c release, PARP cleavage, and the formation of active caspase 3. Sphingolipids 159-172 caspase 3 Homo sapiens 308-317 11483620-6 2001 These results may indicate that a caspase-3 independent signaling pathway is involved in the lysosphingolipid-induced apoptosis and suggest that accumulation of lysosphingolipids, but not parental sphingolipids, triggers the apoptotic cascade in neuronal cells of patients with sphingolipidoses. Sphingolipids 93-109 caspase 3 Homo sapiens 34-43 11483620-6 2001 These results may indicate that a caspase-3 independent signaling pathway is involved in the lysosphingolipid-induced apoptosis and suggest that accumulation of lysosphingolipids, but not parental sphingolipids, triggers the apoptotic cascade in neuronal cells of patients with sphingolipidoses. Sphingolipids 161-178 caspase 3 Homo sapiens 34-43 11483620-6 2001 These results may indicate that a caspase-3 independent signaling pathway is involved in the lysosphingolipid-induced apoptosis and suggest that accumulation of lysosphingolipids, but not parental sphingolipids, triggers the apoptotic cascade in neuronal cells of patients with sphingolipidoses. Sphingolipids 165-178 caspase 3 Homo sapiens 34-43 11313718-2 2001 The transient generation of this sphingolipid mediator preceded cytochrome c release from the mitochondria and activation of the executioner caspase-7 in MCF7 cells which do not express caspase-3. Sphingolipids 33-45 caspase 3 Homo sapiens 186-195 10187863-10 1999 These results suggest that the findings that SNP increased ceramide generation and magnesium-dependent N-SMase activity via caspase-3 are interesting to future study to determine the relation between caspases and sphingolipid metabolites in NO-mediated signaling. Sphingolipids 213-225 caspase 3 Homo sapiens 124-133