PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15492836-3 2004 Addition of MG132 or lactacystin, 1 h prior to the addition of the CDK-inhibitor roscovitine to the cell cultures inhibited apoptosis significantly, as measured by PS exposure, cytokeratin 18 cleavage and caspase-3 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 12-17 caspase 3 Homo sapiens 205-214 16998592-4 2006 DNA fragmentation, mitochondrial membrane depolarization and increased caspase-3-like enzyme activity was exclusively induced only by combined treatment with proteasome inhibitors (epoxomicin, MG132, bortezomib/PS-341) and TRAIL. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 193-198 caspase 3 Homo sapiens 71-80 16337881-7 2006 Interestingly, treatment of hyperoxia-exposed CF cells with two proteasome inhibitors, MG132 and lactacystin, restored p21WAF1/CIP1 protein and was associated with an increase of caspase-3 activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 87-92 caspase 3 Homo sapiens 179-188 15941855-9 2005 The effect of DFMO on TNFalpha/MG132-induced upregulation of caspase-3 activity was reversed by the addition of 100 microM putrescine, confirming that polyamines were really involved in the apoptotic process. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 31-36 caspase 3 Homo sapiens 61-70 15276073-4 2004 Antioxidants, including N-acetylcysteine, inhibited the MG132-induced nuclear damage, loss in mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c and caspase-3 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 56-61 caspase 3 Homo sapiens 176-185 15289872-9 2004 MG132 induced the phosphorylation of ERK at 4 h and thereafter persisted for 8 to 16 h. In contrast, JNK and p38 activation persisted for longer periods and remained enhanced until 24 h. The concomitant activation of effector caspases, caspase-3 and caspase-7 was observed in 786-O cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 236-245 14513055-2 2003 Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 75-81 caspase 3 Homo sapiens 269-294 11477551-11 2001 Although z-DEVD-fmk, a specific caspase-3 inhibitor, suppressed MG132-induced apoptosis in MKN28 cells, it only partially rescued the apoptotic effect in AGS cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 64-69 caspase 3 Homo sapiens 32-41 12239627-0 2002 Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-XS and activation of caspase-3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 76-81 caspase 3 Homo sapiens 170-179 12239627-8 2002 MG132 also caused the release of cytochrome c from mitochondria and the activation of caspase-3 with the consequent degradation of poly-ADP ribose polymerase (PARP). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 86-95 12578613-6 2001 A highly sensitive colorimetric assay was employed and the elevation of caspase-3 activity was detected in both cell lines after treatment with Z-LLL-CHO. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 144-153 caspase 3 Homo sapiens 72-81 11490372-6 2001 MG132 inhibited NF-kappa B binding and enhanced gemcitabine hydrochloride"s inhibition of DNA synthesis (gemcitabine hydrochloride = 73% +/- 1.4% vs gemcitabine hydrochloride + MG132 = 6% +/- 0.4%, P <.05), cell killing (gemcitabine hydrochloride = 87% +/- 2.0 vs gemcitabine hydrochloride + MG132 = 25% +/- 1.3%, P <.05), and caspase-3 activity (gemcitabine hydrochloride = 870 +/- 17.4 vs gemcitabine hydrochloride + MG132 = 1075 +/- 20.4, P <.05). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 333-342 11465715-9 2001 Procaspase 3 processing was enhanced by the proteasome inhibitor MG-132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 65-71 caspase 3 Homo sapiens 0-12 12578613-7 2001 By comparison, these results showed that the leukemic cell line M-07e and KG-1a, which both express bcl-2 at a relative high level, had different susceptibility to undergo apoptosis induced by Z-LLL-CHO, which possibly due to their different levels of expression and activation of caspase-3 precursor, as well as their different degree of bcl-2 cleavage after treated by Z-LLL-CHO. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 193-202 caspase 3 Homo sapiens 281-290 11319608-8 2001 However, in the presence of the proteasome inhibitors MG-132, lactacystin or ALLN we found that cells overexpressing pro-caspase-3 are rapidly targeted for apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 54-60 caspase 3 Homo sapiens 117-130 8694836-3 1996 Unexpectedly, proteasome inhibitors (at 5 microM) such as Z-LLnV, Z-LLL, and lactacystin enhanced CPP32-like activity, Ac-DEVD-MCA degrading activity, in the TNF-treated U937 cells in 3 hr, but E64d, cysteine protease inhibitor, did not. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 66-71 caspase 3 Homo sapiens 98-103 10930537-5 2000 Pretreatment of U937 cells with MG132 or LLnL inhibited etoposide-induced morphological apoptosis and caspase-3 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 32-37 caspase 3 Homo sapiens 102-111 10229667-6 1999 The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 151-160 caspase 3 Homo sapiens 109-118 10554039-11 1999 MG132 also favored the release of cytochrome c from the mitochondria and increased the activity of caspase-3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 99-108 10554039-14 1999 Clear synergistic effects concerning the activation of both caspase-3 and apoptosis were induced by a combination of suboptimal doses of sodium butyrate and MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 157-162 caspase 3 Homo sapiens 60-69 16287099-10 2006 MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 42-51 27091487-6 2016 In cells pretreated with the proteasome inhibitor MG132, CA no longer reversed the 6-OHDA-mediated induction of cleavage of caspase 3 and poly(ADP)-ribose polymerase and no longer reversed the suppression of proteasome activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 50-55 caspase 3 Homo sapiens 124-165 32184020-4 2020 PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 190-195 caspase 3 Homo sapiens 59-67 31687087-6 2019 Treatment with the proteasome inhibitor, MG132, on SCA3-iPSC-derived neurons downregulated proteasome activity, increased production of radical oxygen species (ROS), and upregulated the cleaved caspase 3 level and caspase 3 activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 41-46 caspase 3 Homo sapiens 194-203 31687087-6 2019 Treatment with the proteasome inhibitor, MG132, on SCA3-iPSC-derived neurons downregulated proteasome activity, increased production of radical oxygen species (ROS), and upregulated the cleaved caspase 3 level and caspase 3 activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 41-46 caspase 3 Homo sapiens 214-223 30442180-14 2018 By challenging MNs with a proteasome inhibitor, we found that MNs were more vulnerable to MG132, with some accompanying phenotype changes, such as TDP43 translocation, NF inclusion, mitochondria distribution impairment, and activation of caspase3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 90-95 caspase 3 Homo sapiens 238-246 34002651-8 2021 Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 24-29 caspase 3 Homo sapiens 266-275 33482188-7 2021 MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-6 caspase 3 Homo sapiens 172-180 30488656-11 2019 Treatment of patient cells with MG-132 or staurosporine to induce activation of the intrinsic apoptosis pathway revealed significantly decreased cell viability with increased caspase-3 and caspase-7 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 32-38 caspase 3 Homo sapiens 175-184 30091530-5 2018 SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 9-14 caspase 3 Homo sapiens 77-86 26137056-8 2015 MG-132-induced apoptosis was enhanced by the autophagy inhibitor 3-MA, which may be a result of caspase-3 activation in the EC9706 cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-6 caspase 3 Homo sapiens 96-105 27051056-6 2016 The expression of Caspase3 and Beclin1 was detected by Western blot analysis and reverse transcription-polymerase chain reaction after treatment with 3.0 mug/mL of the cisplatin group and combined treatment with 1.5 mug/mL of MG132 group for 24 hours, respectively. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 226-231 caspase 3 Homo sapiens 18-26 27774335-5 2016 Our results demonstrate that the proteasome inhibitor, MG132, initiates poly(ADP-ribose) polymerase (PARP) cleavage, caspase 3 activation, and nuclear condensation and fragmentation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 55-60 caspase 3 Homo sapiens 117-126 26165741-6 2015 Western blot results showed that MG132 or bortezomib induced high accumulation of ubiquitinated proteins and activation of apoptosis related protein caspase-3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 33-38 caspase 3 Homo sapiens 149-158 27277541-6 2016 The induction of apoptosis by proteasome inhibitor MG132 was mainly through the extrinsic apoptotic pathways of caspase activation such as caspase-8, caspase-3 and PARP cleavage. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 51-56 caspase 3 Homo sapiens 150-159 26648402-8 2016 In addition, MG-132 inhibited the protein expression of the anti-apoptotic protein, B-cell lymphoma (Bcl)-2, whereas the expression levels of Bcl-2-associated X protein and caspase-3 were upregulated. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 13-19 caspase 3 Homo sapiens 173-182 23152053-6 2012 The raise of Bim was accompanied by caspase-3 activation, and a caspase-3 inhibitor reduced MG132-induced apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 92-97 caspase 3 Homo sapiens 64-73 24584782-9 2014 MG132 significantly enhanced cisplatin-induced apoptosis in association with the activation of caspase-3 and -8. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 95-111 23994633-6 2013 The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 42-47 caspase 3 Homo sapiens 109-118 23445492-6 2013 The greatest percentage of apoptosis was obtained with a combination of the drugs; likewise, PTX and MG132 induce G1 phase cell cycle arrest and cleavage of caspases -3,-8, -9 and cytochrome c release and mitochondrial membrane potential loss in U937 human leukemia cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 101-106 caspase 3 Homo sapiens 157-175 22388098-7 2012 Western blotting and/or caspase activity data indicated that PAB downregulated anti-apoptotic Bcl-2 protein and activated caspase-9 and caspase-3, which were largely rescued by NAC or MG-132 (proteasome inhibitor). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 184-190 caspase 3 Homo sapiens 136-145 22791333-9 2012 After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 33-39 caspase 3 Homo sapiens 172-181 22538490-5 2012 Moreover, when compared to wild-type DA neurons, LRRK2-G2019S iPSC-derived DA neurons were more sensitive to caspase-3 activation caused by exposure to hydrogen peroxide, MG-132, and 6-hydroxydopamine. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 171-177 caspase 3 Homo sapiens 109-118 22791147-9 2012 Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 136-141 caspase 3 Homo sapiens 67-76 22310719-3 2012 The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 39-44 caspase 3 Homo sapiens 192-204 22791147-9 2012 Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 136-141 caspase 3 Homo sapiens 199-208 20005289-7 2010 In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in evodiamine-treated A375-S2 cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 13-18 caspase 3 Homo sapiens 58-67 21206980-5 2011 Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 101-106 caspase 3 Homo sapiens 31-40 21297867-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: Here we show that proteasome inhibition with MG132, per se at non-lethal levels, sensitized vascular smooth muscle cells to caspase-3 activation and cell death during ER stress induced by tunicamycin (Tn). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 77-82 caspase 3 Homo sapiens 156-165 20651358-3 2010 MG132 induced cell growth inhibition and apoptosis in HeLa cells, which was accompanied by the loss of mitochondrial membrane potential (MMP; Delta Psi(m)), activation of caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 171-213 20305374-6 2010 Moreover, the combination of celecoxib with MG132 synergistically inhibited cell viability and increased apoptosis, as documented by caspase 3 and 7 activation, PARP cleavage, and down-regulation of Bcl-2. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 44-49 caspase 3 Homo sapiens 133-142 19646807-8 2010 In contrast, MG132 induced classical apoptosis through ROS-mitochondria and subsequent caspase-9/caspase-3 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 13-18 caspase 3 Homo sapiens 97-106 19374806-9 2009 MG-132 treatment decreased the mRNA and protein expression of NF-kappaB, and increased the protein expression of caspase-3. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-6 caspase 3 Homo sapiens 113-122 19374806-10 2009 CONCLUSIONS: MG-132 can induce apoptosis of human erythroleukemia cell line K562 through the down-regulation of NF-kappaB expression and up-regulation of caspase-3 expression. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 13-19 caspase 3 Homo sapiens 154-163 18298651-3 2008 Inhibition of proteasome function by MG-132 in dopaminergic neuronal cell model (N27 cells) rapidly depolarized mitochondria independent of ROS generation to activate the apoptotic cascade involving cytochrome c release, and caspase-9 and caspase-3 activation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 37-43 caspase 3 Homo sapiens 239-248 18298651-4 2008 PKCdelta was a key downstream effector of caspase-3 because the kinase was proteolytically cleaved by caspase-3 following exposure to proteasome inhibitors MG-132 or lactacystin, resulting in a persistent increase in the kinase activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 156-162 caspase 3 Homo sapiens 42-51 18298651-4 2008 PKCdelta was a key downstream effector of caspase-3 because the kinase was proteolytically cleaved by caspase-3 following exposure to proteasome inhibitors MG-132 or lactacystin, resulting in a persistent increase in the kinase activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 156-162 caspase 3 Homo sapiens 102-111 18298651-5 2008 Notably MG-132 treatment resulted in translocation of proteolytically cleaved PKCdelta fragments to mitochondria in a time-dependent fashion, and the PKCdelta inhibition effectively blocked the activation of caspase-9 and caspase-3, indicating that the accumulation of the PKCdelta catalytic fragment in the mitochondrial fraction possibly amplifies mitochondria-mediated apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 8-14 caspase 3 Homo sapiens 222-231 18064564-5 2008 Moreover, MG-132 potentiates the HDACi-induced cell death that was associated with caspase-3 activation, and PARP cleavage. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 10-16 caspase 3 Homo sapiens 83-92 19229559-6 2009 In lymphoblastoid cells carrying SCA8 large alleles, treatment of MG-132 or staurosporine significantly increases the cell death or caspase 3 activity. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 66-72 caspase 3 Homo sapiens 132-141 18492488-4 2008 MG132 and ALLN inhibited the release of cytochrome c from mitochondria into the cytosol in the absence of survival factors and suppressed the cleavage of pro-caspase-9 and -3 to its active forms induced by etoposide. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 0-5 caspase 3 Homo sapiens 154-174