PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26366090-7 2015 Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells. Cisplatin 26-35 caspase 9 Mus musculus 99-108 33646450-5 2021 Cisplatin-induced cell damages were evaluated by TUNEL assay and immunoblot analyses for p53, 14-3-3, Bax, Bcl2, cytochrome C, and activated caspases. Cisplatin 0-9 caspase 9 Mus musculus 141-149 33646450-7 2021 RESULTS: GW0742 suppressed cisplatin-induced apoptosis of mProx cells by reducing the activation of caspase-3 via attenuating the phosphorylation of p53 and 14-3-3, mitochondrial Bax accumulation, cytochrome C release from mitochondria to the cytosol and ensuing cytosolic caspase-9 activation. Cisplatin 27-36 caspase 9 Mus musculus 273-282 33365077-11 2021 In addition, the expression of survivin and XIAP was significantly downregulated, whereas the expression of caspase-3, caspase-7 and caspase-9 was significantly upregulated in tumor tissues from nude mice treated with matrine + cisplatin, compared with those treated with cisplatin, matrine or normal saline. Cisplatin 228-237 caspase 9 Mus musculus 133-142 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. Cisplatin 61-70 caspase 9 Mus musculus 138-145 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. Cisplatin 61-70 caspase 9 Mus musculus 218-227 30469321-5 2018 Western blotting showed that PDQ reversed the CDDP-induced (1) downregulation of Sirtuin-1 (Sirt-1), nuclear-related factor 2 (Nrf2), and Bcl-2, and (2) upregulation of NF-kappaB, Nox-4, Bax, caspase-9, and caspase-3. Cisplatin 46-50 caspase 9 Mus musculus 192-201 29312001-5 2017 Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. Cisplatin 15-24 caspase 9 Mus musculus 82-90 29312001-5 2017 Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. Cisplatin 15-24 caspase 9 Mus musculus 100-108 33045563-8 2020 Moreover, in the renal tissues of LIGHT KO mice, cisplatin-induced mitochondrion injury and the levels of the pro-apoptotic molecules Bax, Cytochrome C (Cyt C), cleaved caspase-3, and cleaved caspase-9 were dramatically increased; in contrast, the expression of anti-apoptotic molecule Bcl-2 was markedly reduced, compared to those in WT mice, suggesting that LIGHT deficiency accelerated cisplatin-induced mitochondrial apoptosis of renal tubular cells in these mice. Cisplatin 49-58 caspase 9 Mus musculus 192-201 32543135-14 2020 Compared with the control group, in the three groups that treated with DDP, the formation of clones and the expression of proliferation marker proteins Ki67 and PCNA were reduce ( P<0.01), while the rate of apoptosis and the expression of apoptosis marker proteins Caspase-3 and Caspase-9 were increased ( P<0.01). Cisplatin 71-74 caspase 9 Mus musculus 279-288 26438401-9 2016 We found that KCa3.1 blockade attenuated cytochrome c release and the increase in the intrinsic apoptotic mediators Bax, Bak, and caspase-9 after cisplatin treatment. Cisplatin 146-155 caspase 9 Mus musculus 130-139 23678002-3 2013 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. Cisplatin 41-45 caspase 9 Mus musculus 98-107 23678002-3 2013 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. Cisplatin 208-212 caspase 9 Mus musculus 98-107 22681485-10 2012 The expression of Bax, caspase-9, and caspase-3 in cisplatin-treated cells were also decreased by PC treatment. Cisplatin 51-60 caspase 9 Mus musculus 23-32 12746256-5 2003 In contrast to p21(+/+) MPTC, cisplatin activated caspase-9 but not caspase-8 in p21(-/-) MPTC before caspase-3 activation. Cisplatin 30-39 caspase 9 Mus musculus 50-59 12746256-9 2003 We conclude that 1) in the presence of p21, cisplatin activates caspase-3 through a mechanism independent of caspase-8 or caspase-9; 2) in the absence of p21, caspase-9 activation precedes caspase-3 activation; 3) the lack of p21 accelerates caspase-3 activation and cisplatin-induced MPTC apoptosis; and 4) MPTC apoptosis is caspase independent in the presence of p21 but partially dependent on caspases in the absence of p21. Cisplatin 44-53 caspase 9 Mus musculus 159-168