PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18641309-9 2008 Indeed, Bid cleavage and cytochrome c release following 15d-PGJ(2) but not MEHP treatment was profoundly inhibited by Z-VAD-FMK, suggesting that 15d-PGJ(2) activates apoptosis via two pathways, Bax mobilization and protease-dependent Bid cleavage. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 118-127 cytochrome c, somatic Homo sapiens 25-37 18662322-3 2008 ENZA-induced apoptosis involved cleavage of caspases 3, 8, and 9 and led to mitochondrial cytochrome c release and was strongly suppressed by the broad spectrum caspase inhibitor zVAD-fmk but only slightly by the expression of the viral caspase 1/8 inhibitor cytokine response modifier-A. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 179-187 cytochrome c, somatic Homo sapiens 90-102 15488639-7 2004 Pre-treatment with a general caspase inhibitor (z-VAD-fmk) prevented cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 48-57 cytochrome c, somatic Homo sapiens 69-81 17136492-4 2007 Hypoxia or TRAIL-induced activation of cathepsins (B, D and L), caspases (-3 and -9), Bid cleavage, release of Bax and cytochrome c, and DNA fragmentation were blocked independently by zVAD-fmk, CA074Me or pepstatin A, consistent with the involvement of lysosomal cathepsin B and D in cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 185-193 cytochrome c, somatic Homo sapiens 119-131 16596338-3 2006 Western blot data demonstrated that cytochrome c (Cyt c), Smac (the second mitochondria-derived activator of caspase), calpain I, caspase-9, -3 and -8 were involved in the apoptotic process, while the pan caspase inhibitor zVAD-fmk almost completely inhibited Dc-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 223-231 cytochrome c, somatic Homo sapiens 36-48 15843890-6 2005 Finally, when cells were pre-treated with caspase inhibitor (z-VAD-fmk) to block caspase activation, the process of Smac release, like that of Cyt-c, was not affected. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 61-70 cytochrome c, somatic Homo sapiens 143-148 14563488-4 2003 Induction of apoptosis was also accompanied by release of cytochrome c, down-regulation of X-linked inhibitor of apoptosis protein (XIAP), and inactivation of Akt, which was blocked by the pan-caspase inhibitor z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 211-220 cytochrome c, somatic Homo sapiens 58-70 15100281-6 2004 Although the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk) decreased DNA fragmentation, cytochrome c release and caspase-9 and caspase-3 activation were not implicated, suggesting that this apoptosis did not primarily involve the intrinsic mitochondrial pathway. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 87-95 cytochrome c, somatic Homo sapiens 126-138 14761678-8 2004 Cytochrome c release was inhibited by zVAD-fmk, however, the inhibition by zIETD-fmk was not complete. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-46 cytochrome c, somatic Homo sapiens 0-12 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 cytochrome c, somatic Homo sapiens 272-284 15469732-4 2004 The broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVADfmk), prevented abrin-triggered caspase activation and partially abolished apoptotic cell death, but did not affect mitochondrial cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 89-96 cytochrome c, somatic Homo sapiens 223-235 12874037-6 2003 Angiostatin(4.5) exposure induced release of cytochrome c from mitochondria in a caspase-dependent manner, but a pan-caspase inhibitor, zVAD-fmk, blocked cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 136-144 cytochrome c, somatic Homo sapiens 154-166 12975347-2 2003 Cells treated with the broad-spectrum caspase inhibitor z-VAD-fmk, caspase-3 (Casp-3)-deficient MCF-7 cells, as well as Bax-deficient DU-145 cells released Smac/DIABLO and cyt-c in response to proapoptotic agents. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 56-65 cytochrome c, somatic Homo sapiens 172-177 12700632-4 2003 Exogenous ROS and caspase-3 induced deltapsi(m) drop and cytochrome c release from mitochondria, which could be prevented by molecular (dominant-negative caspase-9) and pharmacologic (zVAD-fmk) caspase inhibitors and overexpression of Bcl-2. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 184-192 cytochrome c, somatic Homo sapiens 57-69 12640029-5 2003 Partial irradiation of cells expressing cytochrome c-GFP revealed cytochrome c-GFP release from non-irradiated mitochondria at a delayed but unpredictable time interval (between 30 minutes and more than 2.5 hours) following irradiation, which was unaffected by zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 261-269 cytochrome c, somatic Homo sapiens 40-52 11704825-7 2001 Additionally, Z-VAD-fmk, a general inhibitor of caspases which inhibited cytochrome c release in HL-60 and HL-60/VCR cells, had no effect on AIF release in any of these cell lines, but inhibited beta(2)m-induced apoptosis in all three cell lines. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 14-23 cytochrome c, somatic Homo sapiens 73-85 11547546-6 2001 In contrast, in PC60R1R2/Bcl-2 cells cytochrome c release and apoptosis were suppressed by addition of zVAD-fmk or cyclosporin A. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 103-111 cytochrome c, somatic Homo sapiens 37-49 11479221-11 2001 Cytochrome c release was accompanied by dissipation of the mitochondrial transmembrane potential (DeltaPsi(m)), which was partly inhibited by zVAD-fmk, which suggests that caspases are involved in loss of DeltaPsi(m). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 142-150 cytochrome c, somatic Homo sapiens 0-12 11532973-3 2001 This form of apoptosis, inhibited by Z-VAD-fmk, was associated with a loss of mitochondrial potential, a cytosolic release of cytochrome c, activation of caspase-3, degradation of poly(ADP-ribose)polymerase, and internucleosomal DNA fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 37-46 cytochrome c, somatic Homo sapiens 126-138 11121439-7 2000 A broad caspase inhibitor (z-VAD-fmk) blocked the apoptotic morphological changes and the release of cytochrome c. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 27-36 cytochrome c, somatic Homo sapiens 101-113 11281652-8 2001 Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 130-139 cytochrome c, somatic Homo sapiens 29-41 11080180-11 2000 The partial inhibition of cytochrome c release by zVAD-fmk indicates a positive feedback loop that may involve cytochrome c release and zVAD-fmk-sensitive caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-58 cytochrome c, somatic Homo sapiens 26-38 11080180-11 2000 The partial inhibition of cytochrome c release by zVAD-fmk indicates a positive feedback loop that may involve cytochrome c release and zVAD-fmk-sensitive caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-58 cytochrome c, somatic Homo sapiens 111-123 11080180-11 2000 The partial inhibition of cytochrome c release by zVAD-fmk indicates a positive feedback loop that may involve cytochrome c release and zVAD-fmk-sensitive caspases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 136-144 cytochrome c, somatic Homo sapiens 26-38 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 cytochrome c, somatic Homo sapiens 20-32 10913120-8 2000 Bcl-x(L) cooperates with Z-VAD-fmk by blocking the Type II pathway at the level of cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 25-34 cytochrome c, somatic Homo sapiens 83-95 11022849-5 2000 VES triggered the reaction leading to the cleavage of Bid, a member of the death agonist Bcl-2 family, and released cytochrome c (Cyt.c) from the mitochondria into the cytosol by a z-VAD-fmk-inhibitable mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 181-190 cytochrome c, somatic Homo sapiens 116-128 11022849-5 2000 VES triggered the reaction leading to the cleavage of Bid, a member of the death agonist Bcl-2 family, and released cytochrome c (Cyt.c) from the mitochondria into the cytosol by a z-VAD-fmk-inhibitable mechanism. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 181-190 cytochrome c, somatic Homo sapiens 130-135 10702305-5 2000 The addition of the broad-spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) directly after transduction almost completely prevented p53-induced apoptotic cell death but did not inhibit mitochondrial cytochrome c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 104-112 cytochrome c, somatic Homo sapiens 237-249 10702305-7 2000 Cytosolic extracts from Saos-2 cells transduced with p53, but not from Saos-2 cells transduced with the empty adenoviral vector, contained a cytochrome c-releasing activity in vitro, which was still active in the presence of zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 225-233 cytochrome c, somatic Homo sapiens 141-153 10713737-5 2000 Moreover, caspases contributed to the late cyto c release since the caspase inhibitor zVAD prevented only the late but not the early-stage cyto c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 86-90 cytochrome c, somatic Homo sapiens 43-49 10713737-5 2000 Moreover, caspases contributed to the late cyto c release since the caspase inhibitor zVAD prevented only the late but not the early-stage cyto c release. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 86-90 cytochrome c, somatic Homo sapiens 139-145 10713737-9 2000 zVAD prevented the reduction of ATP, Deltapsim, and nuclear condensation when added up to 8 h after IR, at the time the caspases were highly activated but when the majority of cyto c was still maintained in the mitochondria. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-4 cytochrome c, somatic Homo sapiens 176-182 10364179-2 1999 When Jurkat cells were induced to undergo apoptosis by Fas receptor ligation, cytochrome c was released from mitochondria, an event that was prevented by the caspase inhibitor, zVAD-fmk (zVal-Ala-Asp-CH2F). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 177-185 cytochrome c, somatic Homo sapiens 78-90 10798716-5 2000 This change was substantially prevented by Z-VAD-FMK, thereby suggesting that the released cytochrome c might function not only as an initiator but also as an amplifier of the caspase cascade. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 43-52 cytochrome c, somatic Homo sapiens 91-103 10644366-4 2000 Specifically, in HEp-2 cells infected with d120, (i) a broad-range inhibitor of caspase activity, z-vad-FMK, efficiently blocked DNA fragmentation, (ii) cytochrome c was released into the cytoplasm, (iii) caspase-3 was activated inasmuch as poly(ADP-ribose) polymerase was cleaved, and (iv) chromatin condensation and fragmentation of cellular DNA were observed. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 98-107 cytochrome c, somatic Homo sapiens 153-165 10697511-6 1999 Treatment of U937 cells with GGO resulted in the release of cytochrome c from mitochondria prior to DNA fragmentation and the release of cytochrome c was inhibited by Zn2+ ions and by a chelator of Ca2+ ions but not by inhibitors of caspases such as Z-Asp-CH2DCB or Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 266-275 cytochrome c, somatic Homo sapiens 137-149 10528165-8 1999 In addition, cytochrome c release was observed in the in vitro system in the absence or presence of zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 100-108 cytochrome c, somatic Homo sapiens 13-25 9890985-6 1999 Caspase inhibitors, such as endogenous XIAP and synthetic peptide benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk), although capable of altering the kinetics and perhaps mode of cell death, had no influence on this release, suggesting that if cytochrome c plays a role in caspase activation it must precede this step in the apoptotic process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 117-125 cytochrome c, somatic Homo sapiens 255-267 9874570-6 1999 Pretreatment with peptide caspase inhibitors zVAD-FMK or YVAD-CHO prevented GraB apoptosis and cytochrome c release, whereas DEVD-CHO blocked apoptosis but did not prevent cytochrome c release, indicating that caspases act both up- and downstream of mitochondria. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 45-53 cytochrome c, somatic Homo sapiens 95-107 9927051-3 1999 The panspecific inhibitor of caspase activation N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (z-VAD-FMK) prevented all of these events except release of mitochondrial cytochrome c into the cytosol. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 48-103 cytochrome c, somatic Homo sapiens 178-190 9927051-3 1999 The panspecific inhibitor of caspase activation N-benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (z-VAD-FMK) prevented all of these events except release of mitochondrial cytochrome c into the cytosol. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 105-114 cytochrome c, somatic Homo sapiens 178-190 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 cytochrome c, somatic Homo sapiens 74-86 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 cytochrome c, somatic Homo sapiens 288-300 28235426-6 2017 Cell death was (i) mediated by the activation and the cleavage of initiator and executioner caspases; (ii) prevented by the pan-caspase inhibitor z-VAD-fmk; (iii) associated with the release of cytochrome c and with the phosphorylation of members of the mitogen activated protein kinases including p38MAPK, JNK/SAPK and ERK, and (iv) independent of the generation of reactive oxygen species. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 146-155 cytochrome c, somatic Homo sapiens 194-206 9560217-8 1998 In contrast, the broad-specificity caspase inhibitor benzyloxycarbonyl-valinyl-alaninyl-aspartyl-(0-methyl)- fluoromethylketone (zVAD-fmk) and the caspase-inhibiting protein X-IAP had no effect on Bax-induced release of Cyt c from mitochondria in vitro but prevented the subsequent activation of caspases in cytosolic extracts. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 129-137 cytochrome c, somatic Homo sapiens 220-225 34822470-3 2021 Act V-induced apoptosis was characterized by mitochondrial dysfunction, with loss of mitochondria membrane potential (MMP) and cytochrome c release, which then activated cleaved caspase-9, cleaved caspase-3, and cleaved PARP, revealing that it was related to the mitochondrial pathway, and the apoptotic trendency can be reversed by caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 351-360 cytochrome c, somatic Homo sapiens 127-139 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 cytochrome c, somatic Homo sapiens 230-242 24137266-6 2013 The Antp-SMCC-cytochrome c-induced apoptosis was inhibited by z-VAD-fmk, a pan-caspase inhibitor peptide. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 62-71 cytochrome c, somatic Homo sapiens 14-26 22546669-4 2012 Cell death was completely prevented by the non-specific caspase inhibitor z-VAD-fmk and found to be associated with the release of cytochrome c, an increase in the expression of Bax levels and a decrease in the generation of reactive oxygen species. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 74-83 cytochrome c, somatic Homo sapiens 131-143