PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 14562039-4 2003 In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 48-54 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 223-228 31117253-11 2019 When MG132, a potent selective proteasome inhibitor, was utilized, it could restore the Mcl-1 level. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 5-10 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 88-93 12941295-4 2003 The caspase inhibitor Z-VAD.fmk and the proteasome inhibitor MG132 partially protected Mcl-1 from decay, indicating that both caspase-dependent and proteasome pathways are involved during apoptosis. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 61-66 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 87-92 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 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 116-120 34606682-7 2022 Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 101-106 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 41-45 34606682-7 2022 Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 101-106 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 179-183 27421828-9 2016 Furthermore, clitocine regulates Mcl-1 expression at the posttranslational level as no obvious change is observed on mRNA level and proteasome inhibitor MG132 almost blocks the Mcl-1 suppression by clitocine. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 153-158 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 177-182 29074603-7 2018 Decrease in Mcl-1 protein expression was abrogated by treatment with the proteasome inhibitor MG132, and was preceded by downregulation of the Mcl-1 deubiquitinase USP9X, a novel mechanism of Mcl-1 regulation in AML.Conclusions: The data support clinical testing of Pim and FLT3 inhibitor combination therapy for FLT3-ITD AML. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 94-99 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 12-17 28301598-8 2017 Downregulation of Mcl-1 by S6K2 knockdown was partly restored by the proteasome inhibitor MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 90-95 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 18-23 27875574-6 2016 Treatment with MG132, a proteasome inhibitor reduced Mcl-1 degradation stimulated by chidamide. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 15-20 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 53-58 28939105-5 2017 PKCeta depletion had no effect on MCL1 mRNA but the decrease in Mcl-1 by PKCeta knockdown was blocked by proteasomal inhibitors, such as MG132 and lactacystin. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 137-142 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 64-69 28419994-13 2017 Proteasome inhibitor MG132 markedly prevented the degradation of Mcl-1 and blocked bufalin-induced Mcl-1 reduction. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 21-26 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 65-70 28419994-13 2017 Proteasome inhibitor MG132 markedly prevented the degradation of Mcl-1 and blocked bufalin-induced Mcl-1 reduction. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 21-26 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 99-104 24924397-4 2015 Treatment of cells with cycloheximide in the presence of proteasome inhibitor MG132 suggested that Mcl-1 protein levels were regulated at the post-translational step. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 78-83 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 99-104 26087957-10 2015 Furthermore, the effect of MK-2206 on Mcl-1 downregulation was abolished by GSK3beta inhibitor, lithium chloride and proteasome inhibitor, MG-132, suggesting that MK-2206 acted through a GSK3beta-mediated, proteasome-dependent protein degradation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 139-145 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 38-43 25344893-7 2015 Mcl-1 expression was stabilized with MG-132, an inhibitor of proteasomal degradation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 37-43 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 0-5 24261825-5 2013 API-1 treatment decreased the half-life of Mcl-1, whereas inhibition of the proteasome with MG132 rescued Mcl-1 reduction induced by API-1. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 92-97 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 106-111 23703673-10 2013 BI 6727 administration or PLK2 knockdown decreased cellular protein levels of antiapoptotic myeloid cell leukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 173-179 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 92-115 23703673-10 2013 BI 6727 administration or PLK2 knockdown decreased cellular protein levels of antiapoptotic myeloid cell leukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 173-179 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 117-122 23517112-5 2013 RESULTS: Treatment with 0.5-1 muM MG132 alone or 30 ng/mL Bortezomib alone induced a limited apoptosis in MPM cells associated with the elevated Mcl-1 protein level and hyperactive PI3K/Akt signaling. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 34-39 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 145-150 23577147-6 2013 In human breast cancer cells, paclitaxel treatment resulted in MCL-1 degradation which was prevented by a proteasome inhibitor, MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 128-133 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 63-68 21955141-8 2013 The high sensitivity of WERI-Rb to ABT-737 can be increased by downregulating Mcl-1 using the proteasome inhibitor MG-132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 115-121 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 78-83 22078414-9 2011 This dramatic Mcl-1 accumulation was also observed when cells were treated with other two proteasome inhibitors, MG132 and calpain inhibitor I (ALLN). benzyloxycarbonylleucyl-leucyl-leucine aldehyde 113-118 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 14-19 22314265-0 2012 Noxa/Mcl-1 balance influences the effect of the proteasome inhibitor MG-132 in combination with anticancer agents in pancreatic cancer cell lines. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 69-75 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 5-10 22314265-8 2012 The lack of an enhanced apoptosis induction could be correlated with high levels of Mcl-1 in response to the combined treatment with MG-132 and doxorubicin. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 133-139 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 84-89 22314265-9 2012 Thus, the results indicate that regulation of the antiapoptotic and proapoptotic Bcl-2 family members Noxa and Mcl-1 is predicative of the effectiveness of the combination of MG-132 with different anticancer agents on apoptosis induction in pancreatic cancer cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 175-181 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 111-116 22024133-3 2012 Vinblastine treatment of KB-3 cells initially resulted in a phosphatase-sensitive mobility shift in Mcl-1 and then subsequent loss of Mcl-1 protein expression which was prevented by MG132, suggesting that phosphorylation triggered proteosome-mediated degradation. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 182-187 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 134-139 18795123-7 2008 Mcl-1, among the Bcl-2 and IAP (inhibitor of apoptosis protein) antiapoptotic family proteins tested, was proved to be a major inhibitor of the MG132-induced apoptosis in MPM cells. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 144-149 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 0-5 21750559-9 2011 When cells were treated with MG-132, a proteasome inhibitor, Mcl-1 protein level increased. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 29-35 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 61-66 21170508-4 2011 The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 191-196 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 45-50 21170508-4 2011 The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 191-196 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 258-263 17311906-10 2007 Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 50-56 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 116-121 17311906-10 2007 Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 50-56 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 162-167 16672643-6 2006 Furthermore, cotreatment with the proteasome inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) blocked SU9516-mediated Mcl-1 down-regulation, implicating proteasomal degradation in diminished expression of this protein. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 98-103 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 129-134