PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10363899-13 1999 An inhibitor of the caspase-3 (Z-VAD-fmk) reduced apoptosis in both thymus and spleen. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 31-40 caspase 3 Mus musculus 20-29 10754295-2 2000 This up-regulation was completely blocked by the cysteine protease inhibitor Z-VAD-fmk (benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone), whereas DEVD-CHO (succinyl-Asp-Glu-Val-Asp-aldehyde), a caspase 3 inhibitor, had no effect. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 77-86 caspase 3 Mus musculus 195-204 9792795-3 1998 The redistribution of Bax is not inhibited by a caspase inhibitor, zVAD-fmk, which blocks caspase-3 activity and prevents apoptosis in vivo. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 67-75 caspase 3 Mus musculus 90-99 10200549-8 1999 Following IL-3 withdrawal, the caspase inhibitors z-VAD.fmk and boc-asp(OMe)fluoromethylketone (boc-asp.fmk) prevented the cleavage and activation of caspase-3, the breakdown of lamin B1 and partially mitigated PARP degradation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 3 Mus musculus 150-159 29843152-10 2018 Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 80-89 caspase 3 Mus musculus 157-166 9692710-6 1998 Moreover, pretreatment of ventral mesencephalon cultures with the tetrapeptide inhibitors of the caspase-3-like proteases zVAD-FMK or Ac-DEVD-CHO specifically inhibit death of dopamine neurons induced by low concentrations of 1-methyl-4-phenylpyridinium, whereas the caspase-1-like inhibitor Ac-YVAD-CHO was without effect. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 122-130 caspase 3 Mus musculus 97-106 8976202-2 1996 The CPP-32-like protease activity in apoptotic cell lysates was blocked by both the ICE inhibitor Cbz-Val-Ala-Asp(OMe)-fluoromethyl ketone (ZVAD-FMK) as well as its truncated analog Boc-Asp(OMe)-fluoromethyl ketone (BD-FMK), which failed to block ICE. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 98-138 caspase 3 Mus musculus 4-10 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 3 Mus musculus 201-210 31124136-15 2019 Caspase inhibition (Z-VAD-FMK, 50 microm) attenuated cell death with immunostaining for annexin V, cytochrome C, and caspases 3 and 9 pointing to induction of intrinsic apoptosis during H2 O2 exposure. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 20-29 caspase 3 Mus musculus 117-133 31289573-7 2019 Western blotting demonstrated that caspases-3, -8 and -9, and poly(ADP-ribose) polymerase protein levels were increased compared with untreated MA-10 cells; however, the caspase inhibitor, Z-VAD-fmk, reversed these effects. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 189-198 caspase 3 Mus musculus 35-56 8976202-2 1996 The CPP-32-like protease activity in apoptotic cell lysates was blocked by both the ICE inhibitor Cbz-Val-Ala-Asp(OMe)-fluoromethyl ketone (ZVAD-FMK) as well as its truncated analog Boc-Asp(OMe)-fluoromethyl ketone (BD-FMK), which failed to block ICE. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 140-148 caspase 3 Mus musculus 4-10 25737433-7 2015 CFZ and z-VAD-fmk treatments resulted in higher levels of caspase-3 and BAX and lower level of BCL-XL in gastrocnemius muscles and altered the level of proteins in the renin-angiotensin system. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-17 caspase 3 Mus musculus 58-67 28396364-7 2017 In fact, activation of several proapoptotic markers (caspase-9, caspase-3, and PARP) and reversion of the cytotoxic effect upon treatment with an apoptosis inhibitor (Z-VAD-FMK) were observed. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 167-176 caspase 3 Mus musculus 64-73 29931936-0 2017 [Effects of caspase inhibitor z-VAD-fmk on the expressions of calumenin, caspase-3, GRP78 and GRP94 in adriamycin-injured cardiomyocytes]. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 30-39 caspase 3 Mus musculus 73-82 29931936-1 2017 OBJECTIVE: To study the effects of Caspase broad spectrum inhibitor Z-VAD-FMK on the expressions of calumenin,caspase-3, GRP78 and GRP94 in adriamycin-injured cardiomyocytes and to discuss whether there is a regulation relationship between calumenin and endo-plasmic reticulum stress and myocardial apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-77 caspase 3 Mus musculus 110-119 25391371-13 2015 In addition, z-VAD-fmk, a universal inhibitor of caspases, prevented activation of cleavage caspase-3 and abrogates cell death induced by thiostrepton treatment. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 13-22 caspase 3 Mus musculus 92-101 27450912-13 2016 Caspase-3 mRNA expression was 4.75-fold higher in Z-VAD-FMK treated explants compared to control on day 1 (p < 0.001). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 3 Mus musculus 0-9 23446753-9 2013 The apoptosis of Hepa1-6 cells induced by the combination treatment with curcumin and resveratrol was accompanied by caspase-3, -8 and -9 activation, which was completely abrogated by a pan caspase inhibitor, Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 209-218 caspase 3 Mus musculus 117-137 24325816-5 2014 In contrast, blockade of caspase-3 activity by zVADfmk resulted in a significant reduction of cleaved vimentin and secreted vimentin into the culture supernatant. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 47-54 caspase 3 Mus musculus 25-34 24122153-9 2014 Moreover, both 3-MA and necrostatin-1 treatment could suppress cleaved caspase-3 and LC3-II production, whereas zVAD treatment could inhibit caspase-3 cleavage but increased LC3-II protein levels at 72 h after ICH. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 112-116 caspase 3 Mus musculus 141-150 17620508-9 2007 Sustained agonism by beta1AR autoantibodies elicited caspase-3 activation, cardiomyocyte apoptosis, and DCM in vivo, and these processes were prevented by in vivo treatment with the pan-caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 204-213 caspase 3 Mus musculus 53-62 22613767-11 2012 Indeed, zVAD-fmk inhibited effector caspases (caspases-3, -6, -7) as expected but increased caspase-9 cleavage and activity in etoposide-treated MEFs. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-16 caspase 3 Mus musculus 46-64 20861832-4 2011 Treatment of LVS-infected bone-marrow-derived macrophages with a pancaspase inhibitor (zVAD) did not alter bacterial replication, but minimized active caspase-3 and other markers (Annexin V and propidium iodide) of cell death, whereas treatment with both rIL-4 and zVAD resulted in concomitant reduction of both parameters, suggesting that inhibition of bacterial replication by IL-4 was independent of caspase activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 87-91 caspase 3 Mus musculus 151-160 19513564-4 2009 Apoptosis was established as a mechanism of cell death by demonstrating increased production of the p17 activated fragment of caspase-3 by cancer cells in response to Fv-FOXP3 and inhibition of cell killing by the caspase inhibitor, Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 233-242 caspase 3 Mus musculus 126-135 21678460-10 2012 Biselyngbyaside also induced apoptosis accompanied by the induction of caspase-3 activation and nuclear condensation, and these effects were negated by the pancaspase inhibitor z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 177-186 caspase 3 Mus musculus 71-80 19524568-11 2009 p53 and apoptosis markers, caspase-3 and PARP-1 were activated after RGC-5 cells were cultured in glucose-free media for 32 h. Z-VAD-fmk, a pan-caspase inhibitor, was sufficient to prevent apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 127-136 caspase 3 Mus musculus 27-36 16675471-9 2006 Both HA- and RES-induced cleavage of caspase-9 and caspase-3 and PARP were completely blocked by a pan caspase inhibitor, Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 122-131 caspase 3 Mus musculus 51-60 15028782-4 2004 All toxicants induced 8- to 50-fold increases in caspase-3 activities, which were completely inhibited by the pan caspase inhibitor ZVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 132-140 caspase 3 Mus musculus 49-58 15891331-12 2005 The administration of zVAD significantly inhibited myocardial caspase-3 activity and preserved cardiac physiologic function (Langendorff preparation). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-26 caspase 3 Mus musculus 62-71 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 160-169 caspase 3 Mus musculus 29-38 15093249-7 2004 In addition to positive immunoreactivity against the active fragment (p17) of caspase-3, the administration of the pan-caspase inhibitor, zVAD-fmk (40 microM), prevents apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 138-146 caspase 3 Mus musculus 78-87 11781185-7 2001 IFN-gamma-mediated apoptosis is associated with caspase-3 activation that can be prevented by the addition of the broad caspase inhibitor zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 138-146 caspase 3 Mus musculus 48-57 12832530-6 2003 Consequently, cotreatment with a caspase inhibitor (zVAD-fmk) or with an antioxidant (N-acetylcysteine) not only deterred 6-OHDA-induced loss of TH-positive neurons but also abolished the appearance of activated caspase-3 in TH-positive neurons. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 52-60 caspase 3 Mus musculus 212-221 12354286-5 2002 Caspase-3 activation was inhibited by M-CSF treatment to the same degree as with the caspase inhibitor Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 103-112 caspase 3 Mus musculus 0-9 12627324-6 2003 RESULTS: Dose-dependent and time-dependent apoptosis of the cells, concommittant with an activation of caspase-3, were suppressed by the caspase inhibitors zVAD-fmk and zDEVD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 156-164 caspase 3 Mus musculus 103-112 12048029-6 2002 By using specific caspase inhibitors (Ac-DEVD-CHO, Ac-IETD-CHO and zVAD-fmk), we showed that caspase-3 and -7 (DEVDases) are major effector caspases during EV-induced apoptosis in permissive L929 and RK-13 cell cultures. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 67-75 caspase 3 Mus musculus 93-102 11847519-2 2002 The activity of caspase-3 was enhanced during macrophage apoptosis induced by butyrate and the caspase inhibitor z-VAD-FMK (100 microM) inhibited the butyrate effect, indicating the major role of the caspase cascade in the process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 113-122 caspase 3 Mus musculus 16-25 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. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 172-180 caspase 3 Mus musculus 248-257 11488539-8 2001 zVAD-fmk, a broad-spectrum caspase inhibitor, prevented A beta 25-35-induced increase in caspase-3 activity and CEC death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-8 caspase 3 Mus musculus 89-98