PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23540413-5 2013 zVADfmk was used to determine if it could inhibit activation of caspases-2, -3, and -8 in dDCN following 6OHD-mediated stress. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-7 caspase 2 Homo sapiens 64-86 23540413-7 2013 Additionally, WB analysis revealed that caspases-2, -3, and -8 activation was reduced by zVADfmk in 6OHD-treated cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 89-96 caspase 2 Homo sapiens 40-62 11137534-2 2001 A one-day treatment with OA induced accumulation of the 85kDa poly(ADP-ribose) polymerase (PARP) fragment in cell lysates but the response was prevented if cells were treated with OA in the presence of the caspase inhibitors Z-VAD-FMK and Z-DEVD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 225-234 caspase 2 Homo sapiens 206-213 17426447-6 2007 The NG-18-induced apoptosis was blocked completely by a pan-caspase inhibitor Z-VAD-FMK, indicating that caspases were functionally and actively involved in this process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 78-87 caspase 2 Homo sapiens 60-67 17426447-6 2007 The NG-18-induced apoptosis was blocked completely by a pan-caspase inhibitor Z-VAD-FMK, indicating that caspases were functionally and actively involved in this process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 78-87 caspase 2 Homo sapiens 105-113 15825194-6 2005 Pretreatment for 90 min with either the pan-caspase inhibitor Z-VAD-FMK or the caspase-2-selective inhibitor Z-VDVAD-FMK inhibited thapsigargin-stimulated cell death, resulting in the number of viable cells being 115.6% +/- 5.3% (P < 0.001) and 69.3% +/- 2.9% (P < 0.01), respectively, of starting-time control. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 62-71 caspase 2 Homo sapiens 44-51 12907619-6 2003 Proteolytic cleavage of caspase-2, which is poorly inhibited by zVAD-fmk, was concomitant with HDACI-induced death; however, full processing of caspase-2 to the p19 active form was blocked by Bcl-2. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 64-72 caspase 2 Homo sapiens 24-33 23474846-7 2013 Breaking radio-/ chemoresistance in NHL cells using [Bi-213]anti-CD20 depends on caspase activation as demonstrated by complete inhibition of [Bi-213]anti-CD20-induced apoptosis with zVAD.fmk, a specific inhibitor of caspases activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 183-187 caspase 2 Homo sapiens 81-88 15500642-4 2004 The caspase inhibitor zVAD-fmk prevented both the cell detachment and protein cleavage, indicating the function of caspases in these events. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-30 caspase 2 Homo sapiens 4-11 15500642-4 2004 The caspase inhibitor zVAD-fmk prevented both the cell detachment and protein cleavage, indicating the function of caspases in these events. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-30 caspase 2 Homo sapiens 115-123 11137534-6 2001 The possible interference of caspase inhibitors on cell death was also evaluated, and we found that both Z-VAD-FMK and Z-DEVD-FMK could contribute different extents of protection of MCF-7 and HeLa cells from toxic effects caused by OA. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 105-114 caspase 2 Homo sapiens 29-36 9624143-7 1998 Although the specific caspase inhibitory peptides Z-VAD-fmk and Z-DEVD-fmk prevented apoptosis of MCF-7 cells, we were unable to detect activation of caspases 2 and 7, which are known to be inhibited by Z-DEVD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 2 Homo sapiens 22-29 9766499-6 1998 Induction of apoptosis and processing of all the caspases was inhibited by the cell permeable caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 170-179 caspase 2 Homo sapiens 49-57 10772942-4 2000 Here we show that the pan-caspase, tripeptide inhibitor, benzyloxycarbonyl-Val-Ala-Asp (Ome) fluoromethylketone (z-VAD-FMK), inhibited the activation of caspase-2, -3, -7, and -8, and subsequently apoptosis in Jurkat T lymphocytes induced by agonistic anti-Fas. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 113-122 caspase 2 Homo sapiens 26-33 10772942-4 2000 Here we show that the pan-caspase, tripeptide inhibitor, benzyloxycarbonyl-Val-Ala-Asp (Ome) fluoromethylketone (z-VAD-FMK), inhibited the activation of caspase-2, -3, -7, and -8, and subsequently apoptosis in Jurkat T lymphocytes induced by agonistic anti-Fas. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 113-122 caspase 2 Homo sapiens 153-178 10224236-4 1999 The general caspase inhibitor z-VAD-fmk, but not the CPP32 family inhibitor Ac-DEVD-CHO, blocked anti- micro-induced apoptosis, indicating that a caspase not belonging to the CPP32-like family is also implicated in anti- micro-triggered apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 30-39 caspase 2 Homo sapiens 12-19 10224236-4 1999 The general caspase inhibitor z-VAD-fmk, but not the CPP32 family inhibitor Ac-DEVD-CHO, blocked anti- micro-induced apoptosis, indicating that a caspase not belonging to the CPP32-like family is also implicated in anti- micro-triggered apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 30-39 caspase 2 Homo sapiens 146-153 25119188-4 2015 The SAHA-induced cleavage of HSP90 was blocked by a pan-caspase inhibitor, z-VAD-fmk, implying that the process is dependent on caspase activity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 75-84 caspase 2 Homo sapiens 56-63 9343396-8 1997 Furthermore, inhibition of Sp1 cleavage by ZVAD-fmk and ZDEVD-fmk suggests that caspases are directly involved in this event. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 43-51 caspase 2 Homo sapiens 80-88 25119188-4 2015 The SAHA-induced cleavage of HSP90 was blocked by a pan-caspase inhibitor, z-VAD-fmk, implying that the process is dependent on caspase activity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 75-84 caspase 2 Homo sapiens 128-135