PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25066322-6 2014 G226 induced dose-dependent apoptosis of MDA-MB-231 and MCF-7 cells, accompanied by markedly increased activities of caspase-8 and caspase-3/7, which were abolished by caspase inhibitors zVAD or zIETD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 187-191 caspase 8 Homo sapiens 117-126 25521557-8 2015 The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 173-182 caspase 8 Homo sapiens 26-35 25521557-8 2015 The release of caspase-3, caspase-8, and caspase-9 was stimulated by AG4 in CNE, and the decreased proliferation induced by AG4 was blocked by the inhibitor of pan caspase (Z-VAD-FMK). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 173-182 caspase 8 Homo sapiens 15-22 26043797-6 2015 Apoptosis induced by MHY218 was involved in the activation of caspase-8, -9, and -3, and it was blocked by the addition of Z-VAD-FMK, a pan-caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 123-132 caspase 8 Homo sapiens 62-83 25196075-10 2014 However, inhibition of caspases by Z-VAD-FMK reversed the down-regulatory effect of P16 on pAKT (S473) and pP70S6K, as evident by the cell viability assay and flow cytometric analysis but this inhibition did not completely reverse the antiproliferative effect of P16, thereby indicating the role of additional factors apart from caspases in P16 induced apoptosis in MOLT-4 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 35-44 caspase 8 Homo sapiens 23-31 24530510-2 2014 Hence, this study investigated whether an irreversible inhibitor of caspase enzymes, benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone (zVAD-fmk), could be used in post-thaw culture media to increase the survival rate of AFSCs. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 138-146 caspase 8 Homo sapiens 68-75 24973666-7 2014 The general caspase inhibitor, z-VAD-fmk, completely abolished cordycepin-induced cell death, demonstrating that cordycepin-induced apoptosis was dependent on the activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 31-40 caspase 8 Homo sapiens 177-185 24481288-7 2014 The apoptotic cell death induced by CA was accompanied by the activation of caspase-8, -9 and -3, which was completely abrogated by the pan-caspase inhibitor, z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 159-168 caspase 8 Homo sapiens 76-96 24481288-7 2014 The apoptotic cell death induced by CA was accompanied by the activation of caspase-8, -9 and -3, which was completely abrogated by the pan-caspase inhibitor, z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 159-168 caspase 8 Homo sapiens 76-83 24039967-6 2013 Moreover, caspase-8 and caspase-3 activation and PARP-1 cleavage were strongly inhibited/blocked by the addition of the specific caspase inhibitors Z-VAD-FMK and Ac-DEVD-CHO. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 148-157 caspase 8 Homo sapiens 10-19 24398693-4 2014 The caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone greatly diminished caspase 8-dependent NF-kappaB activation induced by Fas ligand (FasL) when c-FLIPL, but not its N-terminal fragment c-FLIP(p43), was expressed. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-75 caspase 8 Homo sapiens 95-104 24337492-9 2014 Furthermore, in the KB oral cancer cells co-stimulation with a caspase inhibitor (Z-VAD-fmk) and Lico-A significantly abolished the apoptotic phenomena. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 82-91 caspase 8 Homo sapiens 63-70 25124618-5 2014 Additionally, MBS treatment led to activation of caspase-9, caspase-8 and caspase-3, and cleavage of PARP, which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 174-183 caspase 8 Homo sapiens 60-69 25036678-5 2014 Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 13-22 caspase 8 Homo sapiens 30-37 25036678-5 2014 Furthermore, z-VAD-fmk (a pan-caspase inhibitor) and z-IETD-fmk (a specific caspase-8 inhibitor) abolished the DHS-induced activation of the caspase-8, -9, and -3, cleavage of PARP, the depolarization of Deltapsim, the release of cytochrome c, the cleavage of Bid, and the downregulation of Bcl-2. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 13-22 caspase 8 Homo sapiens 141-162 21901386-7 2012 Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 112-121 caspase 8 Homo sapiens 26-33 22342732-7 2012 Attenuation of apoptosis in cells pretreated with Z-VAD-FMK suggested the involvement of caspase cascade. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 8 Homo sapiens 89-96 23708311-4 2013 In particular, activation of caspas-3 and caspase-8 as well as release of cytochrome c were significantly enhanced in response to the combined treatment with VA and TNF-alpha (VA/TNF-alpha) and the pan-caspase inhibitor z-VAD-fmk completely reversed the apoptosis, suggesting that caspases are the main effector molecules in VA/TNF-alpha-induced apoptosis via the intrinsic and extrinsic pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 220-229 caspase 8 Homo sapiens 42-51 23708311-4 2013 In particular, activation of caspas-3 and caspase-8 as well as release of cytochrome c were significantly enhanced in response to the combined treatment with VA and TNF-alpha (VA/TNF-alpha) and the pan-caspase inhibitor z-VAD-fmk completely reversed the apoptosis, suggesting that caspases are the main effector molecules in VA/TNF-alpha-induced apoptosis via the intrinsic and extrinsic pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 220-229 caspase 8 Homo sapiens 42-49 23408429-7 2013 In MDA-MB-231 breast cancer cells, sensitization to TRAIL upon MTDH down-regulation was inhibited by the caspase inhibitor Z-VAD-fmk (benzyloxycarbonyl-VAD-fluoromethyl ketone), suggesting that MTDH depletion stimulates activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 123-132 caspase 8 Homo sapiens 234-242 23410748-1 2013 TNF has been reported to induce caspase-independent necroptosis in the presence of Z-VAD-fmk, a pan-caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 83-92 caspase 8 Homo sapiens 32-39 23410748-1 2013 TNF has been reported to induce caspase-independent necroptosis in the presence of Z-VAD-fmk, a pan-caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 83-92 caspase 8 Homo sapiens 100-107 23410748-7 2013 The cleavage of RIP1, which plays a crucial role in TNF-induced necroptosis and is cleaved by caspase-8, was completely inhibited by Z-VAD-fmk or Z-DEVD-fmk, whereas the partial degradation of RIP1 was detected in the presence of Z-Asp-CH2-DCB. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 133-142 caspase 8 Homo sapiens 94-103 23338568-6 2013 Consistently, blockage of caspase activation, through treatment with a caspase inhibitor, z-VAD-fmk, inhibited apoptosis and abrogated Tat-SmacN7 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 90-99 caspase 8 Homo sapiens 26-33 23338568-6 2013 Consistently, blockage of caspase activation, through treatment with a caspase inhibitor, z-VAD-fmk, inhibited apoptosis and abrogated Tat-SmacN7 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 90-99 caspase 8 Homo sapiens 71-78 22644571-4 2012 Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 203-207 caspase 8 Homo sapiens 184-191 22644571-4 2012 Both, tumor necrosis factor alpha and tumor necrosis factor-related apoptosis inducing ligand induced cell death was accompanied by Atg3 cleavage and this event was inhibited by a pan-caspase inhibitor (zVAD) or a caspase-8-specific inhibitor (zIETD). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 203-207 caspase 8 Homo sapiens 214-223 22114764-8 2012 Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked butein-induced activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 46-55 caspase 8 Homo sapiens 94-102 21901386-7 2012 Consistently, blockage of caspase activation, through siRNA knockdown or treatment with a pan-caspase inhibitor z-VAD-fmk, inhibited apoptosis and abrogated SM-164 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 112-121 caspase 8 Homo sapiens 94-101 21341336-5 2011 The apoptosis was obviously inhibited by pretreatment with a general caspase inhibitor, z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 88-97 caspase 8 Homo sapiens 69-76 22159898-10 2012 Moreover, a general caspase inhibitor, Z-VAD-FMK, significantly and almost completely blocked the apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 39-48 caspase 8 Homo sapiens 20-27 19360361-4 2009 A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 25-34 caspase 8 Homo sapiens 6-13 21566207-6 2011 The broad-spectrum caspase inhibitor Z-VAD-fmk and the caspase-9- and caspase-8-specific inhibitors significantly attenuated apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 37-46 caspase 8 Homo sapiens 19-26 21282353-5 2011 Blockage of caspase activation via short interfering RNA knockdown or a pan-caspase inhibitor, z-VAD-fmk, largely abrogated SM-164 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 95-104 caspase 8 Homo sapiens 12-19 21282353-5 2011 Blockage of caspase activation via short interfering RNA knockdown or a pan-caspase inhibitor, z-VAD-fmk, largely abrogated SM-164 radiosensitization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 95-104 caspase 8 Homo sapiens 76-83 21082355-9 2011 ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 110-119 caspase 8 Homo sapiens 92-99 21082355-9 2011 ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 110-119 caspase 8 Homo sapiens 197-206 20136500-6 2010 Since pan-caspase inhibitor z-VAD-fmk abolished the TNF-alpha-induced mitochondrial changes, z-DEVD-fmk, an inhibitor of caspase-3 had no effect, suggesting that TNF-alpha-induced mitochondrial changes or cytochrome c and Smac release requires caspase-8 but not caspase-3 activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 28-37 caspase 8 Homo sapiens 10-17 20580860-6 2010 Z-VAD-fmk and the peptidomimetic inhibitors inhibit caspase-3 and caspase-8 via a three-step kinetic mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 66-75 20580860-7 2010 Inhibition of both caspase-3 and caspase-8 by Z-VAD-fmk and of caspase-3 by the peptidomimetic inhibitors proceeds via two rapid equilibrium steps followed by a relatively fast inactivation step. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 46-55 caspase 8 Homo sapiens 33-42 20195576-8 2010 The effects of the caspase inhibitor, z-VAD-FMK, on the timing of caspase activity are also investigated and are shown to dramatically slow the apoptotic process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-47 caspase 8 Homo sapiens 19-26 20127023-8 2010 The pan-caspase inhibitor, Z-VAD-fmk, partially blocked the cell death induced by KBH-A42. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 27-36 caspase 8 Homo sapiens 8-15 19561399-5 2009 Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-27 caspase 8 Homo sapiens 71-80 19561399-5 2009 Pretreatment with z-VAD-FMK (a pan-caspase inhibitor) or z-IETD-FMK (a caspase-8 inhibitor) blocked TOS/paclitaxel cotreatment-induced PARP cleavage and apoptosis, suggesting that TOS potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in H460 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-27 caspase 8 Homo sapiens 246-255 20696207-8 2010 Caspases were inhibited with zVAD-FMK and zDEVD-FMK; autophagy with 3-methyladenine, LY294002, and wortmannin. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 29-37 caspase 8 Homo sapiens 0-8 20878065-4 2010 The cytotoxic effects of triptolide were significantly inhibited by the caspase inhibitor, z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 91-100 caspase 8 Homo sapiens 72-79 20372860-7 2010 Z-VAD-FMK treatment inhibited, but did not abolish, LVEP-induced apoptosis, indicating that caspases other than caspase-3 participate in this pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 92-100 19360361-4 2009 A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 25-34 caspase 8 Homo sapiens 110-119 19360361-4 2009 A pan-caspase inhibitor, z-VAD-fmk, suppressed this increase in apoptosis and also suppressed the cleavage of caspase-8, caspase-3, and PARP, suggesting a caspase-dependent mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 25-34 caspase 8 Homo sapiens 110-117 17644308-3 2007 In this study, we show that RIP3 is cleaved at Asp328 by caspase-8 under apoptotic stimuli, which is blocked by pan-caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 134-143 caspase 8 Homo sapiens 57-66 18987254-8 2009 Inhibition of caspases by z-VAD-fmk as well as overexpression of Fas-associated death domain-like interleukin-1beta-converting enzyme (FLICE)-like inhibitory proteins FLIP(L) and FLIP(S) to inhibit receptor-mediated apoptosis did not block PV-IgG-induced effects, indicating that apoptosis was not required. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 caspase 8 Homo sapiens 14-22 19167455-3 2009 Involvement of the caspase and the metalloprotease families was confirmed by the observation that their respective broad spectrum inhibitors, Z-VAD-fmk and GM6001, each suppressed HD-induced microvesication. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 142-151 caspase 8 Homo sapiens 19-26 19084044-12 2009 Our experiments with caspase inhibitors Ac-DEVD-CHO, Z-IETD-FMK and Z-VAD-FMK inhibited capsase-3, 8 cleavages but did not prevent OA-induced apoptosis and DNA fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-77 caspase 8 Homo sapiens 21-28 19235152-5 2009 Pretreatment of a pan-caspase inhibitor (benzyloxycarbonyl)-Val-Ala-Asp-(fluoromethyl) ketone (z-VAD-fmk) significantly increases the viability of 1-treated HeLa cells implied that the participation of caspase; Western-blot analysis showed the activation of initiator caspase-8 and caspase-9, and executor caspase-3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 95-104 caspase 8 Homo sapiens 268-277 18359761-8 2008 Pretreatment of cells with caspase inhibitor (Z-VAD-FMK) blocked fisetin-induced activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 46-55 caspase 8 Homo sapiens 95-103 18068200-6 2008 The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 80-89 caspase 8 Homo sapiens 17-26 18068200-6 2008 The 7kCh-induced caspase-8 activity was blocked partially by pre-treatment with z-VAD-fmk and z-IETD-fmk, a caspase-8 inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 80-89 caspase 8 Homo sapiens 108-117 17404499-4 2007 The mechanism of Zvad-induced cell death was proposed to require caspase-8 inhibition. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 17-21 caspase 8 Homo sapiens 65-74 17666813-3 2007 z-VAD-fmk (a broad-caspase inhibitor) almost completely suppressed saucernetin-7-induced DNA ladder formation, thereby implicating the caspase cascade in the apoptotic process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 19-26 15713901-6 2005 Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 77-85 caspase 8 Homo sapiens 25-32 17559898-6 2007 The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 115-124 caspase 8 Homo sapiens 45-66 17559898-6 2007 The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 115-124 caspase 8 Homo sapiens 45-54 17191116-5 2007 Pretreatment with z-VAD-FMK (a pan-caspase inhibitor), z-IETD-FMK (a caspase-8 inhibitor) or z-LEHD-FMK (a caspase-9 inhibitor) blocked TOS and exisulind cotreatment-induced PARP cleavage and apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-27 caspase 8 Homo sapiens 35-42 17007887-9 2006 The experiments using inhibitors of caspases (Z-VAD-FMK, Z-DEVD-FMK and Z-IETD-FMK) confirmed that caspase-3 was involved in the apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 46-55 caspase 8 Homo sapiens 36-44 17062895-5 2006 The underlying mechanism of zVAD-fmk-mediated sensitization to necrotic cell death involves the inhibition of caspase-8-mediated proteolysis of RIP1 and disturbance of the ANT-CypD interaction. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 28-36 caspase 8 Homo sapiens 110-119 15572588-2 2005 In neutrophils, however, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alpha)-induced cell death, and this has been interpreted as evidence for caspase-dependent and -independent cell death pathways. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 62-71 caspase 8 Homo sapiens 44-51 15572588-2 2005 In neutrophils, however, the broad-spectrum caspase inhibitor z-VAD-fmk enhances tumor necrosis factor-alpha (TNF alpha)-induced cell death, and this has been interpreted as evidence for caspase-dependent and -independent cell death pathways. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 62-71 caspase 8 Homo sapiens 187-194 15777082-7 2005 Although ZVAD-sensitive caspase-8 processing occurred in both cell types, pretreatment with either fas-receptor blocking ZB4 or fas-ligand NOK1 neutralizing antibodies did not inhibit HQ-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 9-13 caspase 8 Homo sapiens 24-33 15777082-8 2005 In conclusion, our results demonstrate that HQ induced apoptosis in Jurkat cells occurs via a ZVAD-inhibitable, caspase-dependent process, while in HL-60 cells, apoptosis occurs predominantly via caspase-independent mechanisms. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 94-98 caspase 8 Homo sapiens 112-119 15498850-4 2005 15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 180-184 caspase 8 Homo sapiens 53-60 15498850-4 2005 15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 180-184 caspase 8 Homo sapiens 91-100 15498850-4 2005 15d-PGJ(2)-induced apoptosis occurs through multiple caspase activation pathways involving caspase-8 and caspase-9, and is prevented by pretreatment with the pan-caspase inhibitor ZVAD (z-Val-Ala-Asp). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 180-184 caspase 8 Homo sapiens 91-98 15796160-4 2005 Presence of the pan-caspase inhibitor, Z-VAD-fmk, did not prevent cell detachment, but it did prevent apoptosis of the detached cells indicating that the process of cell detachment, but not apoptosis, is independent of caspase activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 39-48 caspase 8 Homo sapiens 20-27 15474362-2 2004 Several caspase inhibitors, such as the well-known peptidyl inhibitor carbobenzoxy-Val-Ala-Asp-fluoromethylketone (zVADfmk), can protect neurons from apoptotic death caused by mitochondrial toxins. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 115-122 caspase 8 Homo sapiens 8-15 17291719-6 2007 However, inhibition of caspases with zVAD-fmk resulted in strong inhibition of all these signalling pathways in Colo357-BclxL, but enhanced NFkappaB and JNK signalling in PancTuI cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 37-45 caspase 8 Homo sapiens 23-31 16316721-5 2006 Importantly, triptolide induced the appearance of a truncated 23kD Bcl-2 which was inhibited by the general caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 126-135 caspase 8 Homo sapiens 108-115 16007152-5 2005 The broad-specificity caspase inhibitor z-VAD-fmk completely blocked Mcl-1 cleavage induced by PDT, STS or UVC, providing evidence for Mcl-1 as a substrate for caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 40-49 caspase 8 Homo sapiens 160-168 16151646-4 2005 There was minimal effect on MGd-induced apoptosis by the caspase inhibitor z-VAD-fmk, even though caspase-3 activity (as measured by DEVD-cleavage) was completely inhibited. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 75-84 caspase 8 Homo sapiens 57-64 16151646-7 2005 Our results demonstrating differential sensitivity of drug-induced apoptosis to caspase inhibitors suggest that the term "caspase-independent apoptosis" cannot be solely defined as apoptosis that is not inhibited by z-VAD-fmk as has been utilized in some published studies. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 216-225 caspase 8 Homo sapiens 80-87 15547726-6 2004 IFN-gamma-mediated facilitation of apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk and the caspase-8 specific inhibitor zIEDT-fmk, indicating an important role of caspase-8 in mediating sensitation by IFN-gamma in neuroblastoma cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 88-96 caspase 8 Homo sapiens 177-186 15713901-6 2005 Addition of irreversible caspase inhibitors (e.g., the pan-caspase inhibitor zVAD-fmk) to G3139-treated cells almost completely blocked cytotoxicity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 77-85 caspase 8 Homo sapiens 59-66 15379865-3 2004 Cell death could be prevented by the general caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 63-71 caspase 8 Homo sapiens 45-52 15481331-4 2004 Both time- and concentration-dependent effects on apoptosis were noted, which were effectively prevented by the caspase inhibitor z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 130-139 caspase 8 Homo sapiens 112-119 15115612-6 2004 The activity of caspase-3, which is one of the major executioner caspases, was found to be inhibited by both Z-DEVD-MFK and Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 124-133 caspase 8 Homo sapiens 65-73 15258464-5 2004 We demonstrate that 2-MeOE2bisMATE-induced apoptosis of CAL51 breast cancer cells was associated with rapid activation of caspase 3 and 9, but not caspase 8 (as measured by BID cleavage) and was completely prevented by the caspase inhibitor zVADfmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 241-248 caspase 8 Homo sapiens 122-129 15301743-10 2004 Caspase family inhibitor (z-VAD-fmk), caspase-9 inhibitor (Ac-AAVALPAVLLALLAPLEHD-CHO), and caspase-3 inhibitor (z-DEVD-fmk) partially prevented diosgenin-induced apoptosis, but not caspase-8 inhibitor (z-IETD-fmk) and caspase-10 inhibitor (z-AEVD-fmk). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 caspase 8 Homo sapiens 0-7 14644418-4 2003 Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 126-134 caspase 8 Homo sapiens 21-30 14676829-8 2004 EGCG-mediated induction of apoptosis was significantly blocked by the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (Z-VAD-FMK), and moderately blocked by the specific caspase-3 inhibitor Z-DEVD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 88-143 caspase 8 Homo sapiens 70-77 14987955-8 2004 It was confirmed that the activation of caspase 8, 9 and 3 and the cleavage of PARP by heyneanol A were completely blocked by adding Z-VAD-FMK, a caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 133-142 caspase 8 Homo sapiens 40-58 14719107-4 2004 Furthermore, the apoptotic phenotypes totally disappeared with zVAD-fmk, a caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 63-71 caspase 8 Homo sapiens 75-82 14761678-9 2004 The activation of caspase-8 was inhibited not only by zIETD-fmk but also by zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 76-84 caspase 8 Homo sapiens 18-27 14644418-4 2003 Cleavage of Bid, the caspase-8 substrate, was inhibited by the broad caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD-fmk), whereas cytochrome c release was not affected, suggesting that activation of caspase-8 and subsequent Bid cleavage occur downstream of cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 126-134 caspase 8 Homo sapiens 214-223 14508070-6 2003 And the pan-caspase inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone (z-VAD-fmk) and Q-Val-Asp (OMe)-CH(2)-OPH (Q-VD (OMe)-OPH) prevented cell death induced by delta(12)-PGJ(2) showing participation of caspases in this process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 71-80 caspase 8 Homo sapiens 12-19 12969378-5 2003 Low alpha-toxin doses (3-30 ng ml-1) dose- and time-dependently induced apoptosis in both cell types, which was completely blocked by the caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 156-164 caspase 8 Homo sapiens 138-145 14508522-5 2003 Induction of apoptosis was accompanied by caspase-8 and caspase-9 activation, and could be blocked by treatment with the caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 139-148 caspase 8 Homo sapiens 42-51 12663669-5 2003 The caspase inhibitor zVADfmk completely blocks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents loss of DeltaPsi and cell death for cytokine plus cycloheximide treatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-29 caspase 8 Homo sapiens 4-11 12837490-9 2003 In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 8 Homo sapiens 32-39 12837490-9 2003 In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 8 Homo sapiens 127-135 12837490-9 2003 In addition, the broad spectrum caspase inhibitor z-VAD-fmk inhibited both the appearance of PS exposure and the activation of caspases, illustrating the functional relevance of caspase activation during HP-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 8 Homo sapiens 127-134 12663669-5 2003 The caspase inhibitor zVADfmk completely blocks caspase activation, DNA degradation, and nuclear fragmentation in both cases but only prevents loss of DeltaPsi and cell death for cytokine plus cycloheximide treatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-29 caspase 8 Homo sapiens 48-55 12669310-10 2003 Moreover, the general caspase inhibitor ZVAD blocked the cleavage and activation of most caspases tested except caspase-9. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 40-44 caspase 8 Homo sapiens 89-97 12393608-4 2003 Here, we found that inhibition of caspases by the general caspase inhibitor zVAD-fmk did not prevent TNF-alpha-induced PMN death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 76-84 caspase 8 Homo sapiens 34-42 12393608-4 2003 Here, we found that inhibition of caspases by the general caspase inhibitor zVAD-fmk did not prevent TNF-alpha-induced PMN death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 76-84 caspase 8 Homo sapiens 34-41 12417974-7 2003 Supplementation of z-VAD-fmk, a general caspase inhibitor, provided short-term protection against gentamicin-induced hair cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 19-28 caspase 8 Homo sapiens 40-47 12661987-7 2003 The apoptotic process was almost completely blocked in the presence of the general caspase inhibitor zVAD.fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 101-105 caspase 8 Homo sapiens 83-90 12576463-5 2003 Involvement of caspases was determined by immunoblot analysis and cell death detection assays after treatment with synthetic inhibitor z-Val-Ala-Asp-fluoromethyl ketone, z-DEVD-fmk, or z-IETD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 135-168 caspase 8 Homo sapiens 15-23 12504792-5 2003 Since the pan-caspase inhibitor zVAD-fmk did not reduce lysosomal and mitochondrial destabilization, these events occur upstream of caspase activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 32-40 caspase 8 Homo sapiens 14-21 12504792-5 2003 Since the pan-caspase inhibitor zVAD-fmk did not reduce lysosomal and mitochondrial destabilization, these events occur upstream of caspase activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 32-40 caspase 8 Homo sapiens 132-139 11840266-5 2002 Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 106-114 caspase 8 Homo sapiens 14-22 12181741-5 2002 MMC treatment led to pronounced caspase-8, -9, and -7 processing and early morphological features of apoptosis within 48 h. This could be inhibited by the broad-spectrum caspase inhibitor z-VAD.fmk and to a lesser extent by z-IETD.fmk and z-LEHD.fmk, which have a certain preference for inhibiting caspase-8 and -9, respectively. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 188-197 caspase 8 Homo sapiens 298-314 12170777-8 2002 Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by > 90%. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-65 caspase 8 Homo sapiens 14-21 12170777-8 2002 Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by > 90%. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-65 caspase 8 Homo sapiens 43-50 12170777-8 2002 Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by > 90%. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-65 caspase 8 Homo sapiens 162-171 12170777-8 2002 Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24 h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by > 90%. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-65 caspase 8 Homo sapiens 287-295 11795493-5 2001 zVAD-Fmk, a universal inhibitor of caspases, kept the caspase-3 from being activated but not caspase-9. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-8 caspase 8 Homo sapiens 35-43 11595831-4 2001 Pretreatment of T lymphocytes with caspase inhibitors Z-VAD.fmk or DEVD.fmk prevented DNA fragmentation in response to TPEN indicating that apoptosis triggered by zinc deficiency is entirely dependent on activation of caspase family members. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 54-63 caspase 8 Homo sapiens 35-42 12466493-8 2002 Second, both irreversible caspase inhibitors, z-DEVD-FMK and z-VAD-FMK, delayed MVV-induced cellular lysis as well as virus growth. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-70 caspase 8 Homo sapiens 26-33 12357364-4 2002 Co-treatment of cells with the pan-caspase inhibitor Z-VAD-fmk attenuated some morphological and biochemical characteristics of apoptosis and delayed 2CdA-induced DeltaPsi(m) loss, but did not prevent cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 53-62 caspase 8 Homo sapiens 35-42 11992538-9 2002 Furthermore, Apo2L/TRAIL-induced apoptosis and its augmentation by chemotherapy was effectively inhibited by caspase-8 zIETD-fmk and caspase-3 zDEVD-fmk protease inhibitors and by the pan-caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 206-214 caspase 8 Homo sapiens 109-118 11846806-7 2002 The DENSPM-induced cell death was dependent on the activation of the caspases as it was inhibited by the general caspase inhibitor Z-Val-Ala-Asp fluoromethyl ketone. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 131-164 caspase 8 Homo sapiens 69-77 11846806-7 2002 The DENSPM-induced cell death was dependent on the activation of the caspases as it was inhibited by the general caspase inhibitor Z-Val-Ala-Asp fluoromethyl ketone. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 131-164 caspase 8 Homo sapiens 69-76 11859461-5 2002 The cell death by DMHS was partially prevented by the caspase inhibitor, zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 73-81 caspase 8 Homo sapiens 54-61 11840266-5 2002 Activation of caspases was necessary for ajoene-induced apoptosis since the broad-range caspase inhibitor zVAD-fmk completely abrogated ajoene-mediated DNA fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 106-114 caspase 8 Homo sapiens 14-21 11410864-2 2001 JNK activation was completely dependent on the activation of caspases in type I and type II cells, as revealed by the inhibitory effects of the caspase inhibitors zVAD-fmk or the cowpoxvirus-encoded CrmA protein. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 163-171 caspase 8 Homo sapiens 61-69 11410864-2 2001 JNK activation was completely dependent on the activation of caspases in type I and type II cells, as revealed by the inhibitory effects of the caspase inhibitors zVAD-fmk or the cowpoxvirus-encoded CrmA protein. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 163-171 caspase 8 Homo sapiens 61-68 11070498-7 2000 Furthermore, we showed that the caspase inhibitor z-VAD-fmk inhibited DNA fragmentation, but only partially inhibited the appearance of apoptotic morphology. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 8 Homo sapiens 32-39 10970901-5 2000 Caspase inhibitors suppressed the DNA fragmentation in the order of Z-VAD-FMK > caspase-8 inhibitor > caspase-3 inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-77 caspase 8 Homo sapiens 83-92 11350795-3 2001 TNF-alpha also triggered endothelial cell apoptosis beginning at 4 h, which was attenuated by the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 116-148 caspase 8 Homo sapiens 98-105 11355877-6 2001 However, 100 microM Z-VAD.fmk, a pan caspase inhibitor, completely blocked TRAIL-initiated mitochondrial alterations and cleavages of caspases and Bid. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 20-29 caspase 8 Homo sapiens 37-44 11355877-6 2001 However, 100 microM Z-VAD.fmk, a pan caspase inhibitor, completely blocked TRAIL-initiated mitochondrial alterations and cleavages of caspases and Bid. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 20-29 caspase 8 Homo sapiens 134-142 11381362-7 2001 Apoptosis induction in HT29 cells was concomitant with processing of caspases 3, 7, 8, and 9 and was inhibited by the caspase inhibitor ZVAD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 136-140 caspase 8 Homo sapiens 69-77 11381362-7 2001 Apoptosis induction in HT29 cells was concomitant with processing of caspases 3, 7, 8, and 9 and was inhibited by the caspase inhibitor ZVAD. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 136-140 caspase 8 Homo sapiens 69-76 11223917-5 2001 The MPP(+)-induced apoptosis was completely prevented by the broad caspase inhibitor zVAD.fmk but not by the caspase-8 inhibitor IETD.fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 85-89 caspase 8 Homo sapiens 67-74 10793331-7 2000 The pretreatment of cells with pan-caspase inhibitor Z-VAD-fmk markedly prevented CBDCA-mediated cytotoxicity/apoptosis and the modulation of Bcl-2 family proteins (generation of p18 Bax-alpha and p16 Bcl-x(L) ) with only slight prevention of decline of Deltapsi(m). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 53-62 caspase 8 Homo sapiens 35-42 10913120-6 2000 Death induced in the presence of Z-VAD-fmk was associated with a partial inhibition of caspase-8, whereas no effects on cytochrome c release, DEVDase activity, and intranucleosomal DNA cleavage were observed. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 33-42 caspase 8 Homo sapiens 87-96 10913120-7 2000 Thus, Z-VAD-fmk is likely weakening the death-inducing signaling complex-mediated activation of caspase-8 and diverting cells to a Type II pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 6-15 caspase 8 Homo sapiens 96-105 10849426-4 2000 We found that benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), a broad-spectrum caspase inhibitor, mostly inhibited ASK1-induced cell death, suggesting that caspases are required for ASK1-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 65-73 caspase 8 Homo sapiens 170-178 10871865-6 2000 The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 164-173 caspase 8 Homo sapiens 90-99 10871865-6 2000 The first pathway is utilized by lymphoid cells stimulated through Fas, is abrogated in a caspase-8-deficient T-cell line, and is blocked by the caspase inhibitors Z-VAD-fmk and Boc-D-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 164-173 caspase 8 Homo sapiens 90-97 11042678-4 2000 Furthermore, a caspase-8-negative, Fas-resistant Jurkat cell line was sensitive to resveratrol-induced apoptosis which could be strongly inhibited in the Jurkat as well as in the CEM cell line by z-VAD-fmk and z-IETD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 196-205 caspase 8 Homo sapiens 15-24 11210827-6 2000 A broad-spectrum caspase inhibitor, z-VAD-fmk, completely prevented all apoptotic changes, except for the depletion of delta psi m. Both Ac-DEVD-CHO and Ac-IETD-CHO, inhibitors of caspase -3 and -8, respectively, effectively inhibited typical chromatin condensation to almost the same extent. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 36-45 caspase 8 Homo sapiens 17-24 10749135-6 2000 This conclusion is supported by the observation that in HL-60/Apaf-1 cells, ectopic expression of dominant negative caspase-9, its inhibitory short isoform caspase-9b, or XIAP or treatment with the caspase inhibitor zVAD (50 microM) inhibited Apaf-1-induced caspase-8 and Bid cleavage, mitochondrial deltapsim, release of cyt c, and apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 216-220 caspase 8 Homo sapiens 116-123 10399962-11 1999 Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-72 caspase 8 Homo sapiens 14-21 10399962-11 1999 Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-72 caspase 8 Homo sapiens 50-57 10399962-11 1999 Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-72 caspase 8 Homo sapiens 175-183 8681377-3 1996 FLICE binds to the death effector domain of FADD and upon overexpression induces apoptosis that is blocked by the ICE family inhibitors, CrmA and z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 146-155 caspase 8 Homo sapiens 0-5 10066378-4 1999 We demonstrate that cytochrome c is released from mitochondria of Jurkat cells in response to both staurosporine and an agonistic anti-Fas antibody and that only the latter is inhibited by the caspase inhibitor z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 211-220 caspase 8 Homo sapiens 193-200 10022243-3 1998 The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 80-89 caspase 8 Homo sapiens 4-11 10022243-3 1998 The caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone (Z-VAD.fmk) blocked the activation of caspases, PS exposure and the reduction in delta psi(m) as well as the morphological changes associated with apoptosis but it did not inhibit the release of mitochondrial cytochrome c. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 80-89 caspase 8 Homo sapiens 117-125 9830064-6 1998 In these cells, TRAIL-induced cell death and activation of the apoptosis executioner caspase-8 (FLICE/MACH) and caspase-3 (YAMA, CPP-32, Apopain), that belong to caspase subfamily of cysteine proteases, were abrogated, whereas JNK activation remained unaffected and was still sensitive toward z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 293-302 caspase 8 Homo sapiens 85-94 9830064-6 1998 In these cells, TRAIL-induced cell death and activation of the apoptosis executioner caspase-8 (FLICE/MACH) and caspase-3 (YAMA, CPP-32, Apopain), that belong to caspase subfamily of cysteine proteases, were abrogated, whereas JNK activation remained unaffected and was still sensitive toward z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 293-302 caspase 8 Homo sapiens 85-92 9743944-4 1998 Drug-induced apoptosis critically depends on activation of caspases since apoptosis is almost completely abrogated by the caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 140-148 caspase 8 Homo sapiens 59-67 9743944-4 1998 Drug-induced apoptosis critically depends on activation of caspases since apoptosis is almost completely abrogated by the caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 140-148 caspase 8 Homo sapiens 59-66 9184224-10 1997 Activation of FLICE is blocked by the peptide inhibitors zVAD-fmk, zDEVD-fmk and zIETD-fmk, but not by crmA or Ac-YVAD-CHO. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 57-65 caspase 8 Homo sapiens 14-19 10207055-11 1999 Furthermore, an increase of rhodamine-123 uptake into intact cells, which has been explained by mitochondrial swelling, occurred considerably later than the caspase activation and was blocked by Z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 195-204 caspase 8 Homo sapiens 157-164 10194469-2 1999 The Cer response to all three stimuli was mapped in between caspases sensitive to benzoyloxycarbonyl-VAD-fluoromethylketone (zVAD-fmk) and acetyl-DEVD-aldehyde (DEVD-CHO). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 125-133 caspase 8 Homo sapiens 60-68 9988752-6 1999 However, Z-VAD.FMK inhibits chemical-induced apoptosis at a stage after commitment to cell death by inhibiting the initiator caspase-9 and the resultant postmitochondrial activation of effector caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 9-18 caspase 8 Homo sapiens 194-202 10050884-5 1999 Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 173-181 caspase 8 Homo sapiens 78-86 10050884-5 1999 Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 173-181 caspase 8 Homo sapiens 78-85 9847376-3 1999 Incubation of infected cells with the peptide inhibitor z-VAD-fmk abrogated SV-induced apoptosis, indicating that proteases of the caspase family were involved. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 56-65 caspase 8 Homo sapiens 131-138 34466155-8 2021 Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 158-167 caspase 8 Homo sapiens 139-146 34466155-8 2021 Flow cytometry and western blot analyses demonstrated that pioglitazone-mediated apoptosis was blocked following pretreatment with the pan-caspase inhibitor, z-VAD-fmk, indicating that pioglitazone-induced apoptosis was mediated via a caspase-dependent signaling pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 158-167 caspase 8 Homo sapiens 235-242 35393392-7 2022 Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 178-202 caspase 8 Homo sapiens 160-167 35393392-7 2022 Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 178-202 caspase 8 Homo sapiens 280-287 35393392-7 2022 Co-treatment with specific necroptosis inhibitor necrostatin-1 (Nec-1) or Necrosulfonamide (NSA) prevented cell death caused by iPA treatment while the general caspase inhibitor Z-VAD-fluoromethylketone (z-VAD-fmk) did not elicit any effect, suggesting that this molecule induces caspase-independent necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 204-213 caspase 8 Homo sapiens 160-167 33841010-11 2021 Z-VAD-FMK inhibited caspase activation and significantly reversed GRh2-induced apoptosis and PML-RARA degradation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 20-27 33841010-6 2021 Z-VAD-FMK, LY294002, and C 87, as inhibitors of caspase, and the phosphatidylinositol 3-kinase (PI3K) and tumor necrosis factor-alpha (TNF-alpha ) pathways were used to clarify the relationship between GRh2-induced apoptosis and PML-RARA degradation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 48-55 32539919-5 2020 Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 13-20 33108350-4 2020 Here, we show that knockdown of CASP8 renders HNSCCs susceptible to necroptosis by a second mitochondria-derived activator of caspase (SMAC) mimetic, Birinapant, in combination with pan-caspase inhibitors zVAD FMK or Emricasan and radiation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 205-213 caspase 8 Homo sapiens 32-37 33073770-7 2020 MHY2256-induced apoptosis was involved in the activation of caspase-8, -9, and -3 and was prevented by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 121-130 caspase 8 Homo sapiens 60-81 32145587-7 2020 Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 73-82 caspase 8 Homo sapiens 30-37 32145587-7 2020 Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 73-82 caspase 8 Homo sapiens 97-104 32145587-7 2020 Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 84-88 caspase 8 Homo sapiens 30-37 32145587-7 2020 Interestingly, DSF/Cu induced caspase-3 activation was partly blocked by Z-VAD-FMK (zVAD), a pan-caspase inhibitor, indicating at caspase-dependent and -independent paths involved in DSF/Cu induced myeloma cell apoptosis machinery. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 84-88 caspase 8 Homo sapiens 97-104 32539919-5 2020 Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 8 Homo sapiens 91-100 26448608-3 2016 Chal-24 treatment significantly enhanced TRAIL-induced activation of caspase-8 and caspase-3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan-caspase inhibitor z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 210-219 caspase 8 Homo sapiens 69-78 30556589-3 2019 In this study, CA-induced apoptotic cell death resulted in the activation of the caspase-8-mediated caspase cascade, as evidenced by the cleavage of the substrate protein Bid and the caspase-8 inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 203-212 caspase 8 Homo sapiens 81-90 30556589-3 2019 In this study, CA-induced apoptotic cell death resulted in the activation of the caspase-8-mediated caspase cascade, as evidenced by the cleavage of the substrate protein Bid and the caspase-8 inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 203-212 caspase 8 Homo sapiens 183-192 32186020-12 2019 YGJDSJ-induced apoptosis was completely abrogated by a pan caspase inhibitor, Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 78-87 caspase 8 Homo sapiens 59-66 30668391-10 2019 Blockade of caspases with Z-VAD-FMK converted apoptosis-related proteins. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 caspase 8 Homo sapiens 12-20 29128513-11 2018 DHA-induced apoptotic cell death, activation of caspases and cleavage of PARP were dramatically inhibited by pan caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 131-140 caspase 8 Homo sapiens 48-56 30107166-9 2018 Luteolin led a significantly increase in apoptosis accompanied by activation of caspase 8, -9 and -3 and cleavage of poly (ADP-ribose) polymerase (PARP), which was completely blocked by Z-VAD-FMK, a pan caspase inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 186-195 caspase 8 Homo sapiens 80-100 30008897-9 2018 Treatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk, a pan-caspase inhibitor) almost completely blocked metformin-induced apoptosis and degradation of c-FLIPL protein. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 66-75 caspase 8 Homo sapiens 83-90 27752362-8 2016 Regarding the inhibitors, z-VAD-fmk diminishes the cleaved caspase 8, RIP1, RIP3, and MLKL induced by Tan IIA, and reconstructs the ripoptosome complex, which marks cells moving from apoptosis to necroptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 caspase 8 Homo sapiens 59-68 27695262-12 2016 Furthermore, KA-induced DNA fragmentation was abolished by pretreatment with z-VAD-FMK (a broad caspase inhibitor), z-DEVD-FMK (a caspase-3 inhibitor), and z-IETD-FMK (a caspase-8 inhibitor), but not by z-LEHD-FMK (a caspase-9 inhibitor) pretreatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 77-86 caspase 8 Homo sapiens 96-103 26912071-8 2016 Addition of the broad-range caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD.fmk) significantly protects RCC cells against BV6/IFNalpha-induced apoptosis, demonstrating that caspase activity is required for apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 98-106 caspase 8 Homo sapiens 28-35 26375985-7 2016 A pan inhibitor of caspases, Z-VAD-FMK (20 muM), blocked caspase-mediated mitochondrial membrane depolarization. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 29-38 caspase 8 Homo sapiens 19-27