PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10200338-7 1999 WAF1, c-myc and Bax mRNAs were also induced by doxorubicin in the WT cells but not in the Y8 cells. Doxorubicin 47-58 BCL2-associated X protein Mus musculus 16-19 15380639-9 2004 Apoptosis was manifested by elevation of bax and bad mRNA levels, which was much more rapid and intense in the case of free doxorubicin and HYD conjugate. Doxorubicin 124-135 BCL2-associated X protein Mus musculus 41-44 11759827-7 2001 Doxorubicin treatment induced Bax expression and down-regulated Bcl-2 expression. Doxorubicin 0-11 BCL2-associated X protein Mus musculus 30-33 15389801-10 2005 Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation. Doxorubicin 73-84 BCL2-associated X protein Mus musculus 203-206 14766674-2 2004 Administration of DOX (22.5 mg/kg ip) in mice upregulated the mRNA levels of Bax and MDM2, whereas PFT-alpha attenuated those levels when administered at a total dose of 4.4 mg/kg at 30 min before and 3 h after DOX challenge. Doxorubicin 18-21 BCL2-associated X protein Mus musculus 77-80 14766674-5 2004 The protein levels of Bax and MDM2 were elevated by DOX and attenuated by PFT-alpha. Doxorubicin 52-55 BCL2-associated X protein Mus musculus 22-25 34964693-7 2022 The PEG-EV-DOX administration in vivo reduced NF-kappaB activation and increased BAX expression, suggesting better prognosis of EV-based therapy than liposomal DOX treatment. Doxorubicin 11-14 BCL2-associated X protein Mus musculus 81-84 34964693-7 2022 The PEG-EV-DOX administration in vivo reduced NF-kappaB activation and increased BAX expression, suggesting better prognosis of EV-based therapy than liposomal DOX treatment. Doxorubicin 160-163 BCL2-associated X protein Mus musculus 81-84 34760256-9 2021 In addition, we observed NMCP-2 inhibited the activation of the mitochondrial apoptosis pathway and regulated the disordered expression of Bcl-2 and Bax in the myocardial tissues of DOX-treated mice. Doxorubicin 182-185 BCL2-associated X protein Mus musculus 149-152 34192626-4 2021 Cellular experiments show that Dox-loaded self-assembled messenger RNA nanospheres (mRNA-NSs@Dox) can reduce the viability of 4 T1 breast cancer cells by significantly upregulating Bax protein, thereby inducing the activation of Caspase 3 in 4 T1 cells. Doxorubicin 31-34 BCL2-associated X protein Mus musculus 181-184 34192626-4 2021 Cellular experiments show that Dox-loaded self-assembled messenger RNA nanospheres (mRNA-NSs@Dox) can reduce the viability of 4 T1 breast cancer cells by significantly upregulating Bax protein, thereby inducing the activation of Caspase 3 in 4 T1 cells. Doxorubicin 93-96 BCL2-associated X protein Mus musculus 181-184 32882870-12 2020 FKB+doxorubicin-mediated dysregulated Bax/Bcl-2, Beclin-1/Bcl-2 ratios suggested apoptosis, autophagy induction in AGS cells. Doxorubicin 4-15 BCL2-associated X protein Mus musculus 38-41 32699841-10 2019 Moreover, DOX caused a 49% decline in cardiac BCL2/BAX expression, which was restored with RIPC (p < 0.05 vs. DOX). Doxorubicin 10-13 BCL2-associated X protein Mus musculus 51-54 32776015-0 2020 A small-molecule allosteric inhibitor of BAX protects against doxorubicin-induced cardiomyopathy. Doxorubicin 62-73 BCL2-associated X protein Mus musculus 41-44 32776015-2 2020 Here we show that BAX is rate-limiting in doxorubicin-induced cardiomyopathy and identify a small-molecule BAX inhibitor that blocks both apoptosis and necrosis to prevent this syndrome. Doxorubicin 42-53 BCL2-associated X protein Mus musculus 18-21 32776015-6 2020 This study identifies BAX as an actionable target for doxorubicin-induced cardiomyopathy and provides a prototype small-molecule therapeutic. Doxorubicin 54-65 BCL2-associated X protein Mus musculus 22-25 31534548-13 2019 The results suggested that the anticancer molecular mechanism of the combination therapy of glycyrrhizin and doxorubicin in ALG NGPs was performed via regulating apoptosis pathway of Bax/Bcl-2 ratio and caspase-3 activity, which was also verified in H22 tumor-bearing mice. Doxorubicin 109-120 BCL2-associated X protein Mus musculus 183-186 30734460-7 2019 In addition, DOX downregulated survival proteins (p-Akt, Bcl-2) with concomitant upregulation in Erk (1/2), Bax and cleaved caspase-3 expressions. Doxorubicin 13-16 BCL2-associated X protein Mus musculus 108-111 30224925-14 2018 DOX significantly decreased Bax and increased cytochrome c expressions in the cytoplasm, whereas Bax was upregulated and cytochrome c was downregulated in the mitochondria, which were reversed by SYKT treatment. Doxorubicin 0-3 BCL2-associated X protein Mus musculus 28-31 30622447-7 2018 Pretreatment with LDR significantly prevented DOX-induced cardiotoxicity likely through preventing DOX-induced mitochondrial Bcl2/Bax dyshomeostasis-induced caspase-3 cleavage-dependent apoptosis. Doxorubicin 46-49 BCL2-associated X protein Mus musculus 130-133 30622447-7 2018 Pretreatment with LDR significantly prevented DOX-induced cardiotoxicity likely through preventing DOX-induced mitochondrial Bcl2/Bax dyshomeostasis-induced caspase-3 cleavage-dependent apoptosis. Doxorubicin 99-102 BCL2-associated X protein Mus musculus 130-133 30361442-7 2018 We also found that DOX-induced CDK2 activation in the mouse heart is associated with up-regulation of the pro-apoptotic BCL2 family member BCL2-like 11 (Bim), a BH3-only protein essential for triggering Bax/Bak-dependent mitochondrial outer membrane permeabilization. Doxorubicin 19-22 BCL2-associated X protein Mus musculus 203-206 29416617-6 2018 Pretreatment of DOX-treated mice with LDR also decreased DOX-induced cardiac cell apoptosis (TUNEL staining and cleaved caspase-3) and mitochondrial apoptotic pathway (increased p53, Bax, and caspase-9 expression and decreased Bcl2 expression and DeltaPsim dissipation). Doxorubicin 16-19 BCL2-associated X protein Mus musculus 183-186 28922986-12 2017 In connection with that, DIM significantly attenuated DOX-induced apoptosis by upregulation of Bcl-2 expression and downregulation of Bax and caspase-3 expression. Doxorubicin 54-57 BCL2-associated X protein Mus musculus 134-137 26450947-5 2016 Intriguingly, resveratrol attenuated the doxorubicin-induced elevations of apoptotic and catabolic markers measured as Bax, caspase 3 activity, apoptotic DNA fragmentation, MuRF-1, ubiquitinated proteins, and proteasomal activity in aged muscles, whereas these beneficial effects were abolished on inhibition of sirtuin 1 by sirtinol or EX527. Doxorubicin 41-52 BCL2-associated X protein Mus musculus 119-122 28560697-10 2017 Western blot analysis indicated that the expression level of cardiac caspase-3, caspase-8, Bax and BNIP3 were up-regulated due to DOX injection (9 mg/kg). Doxorubicin 130-133 BCL2-associated X protein Mus musculus 91-94 26722406-14 2015 Severe apoptosis in doxorubicin group was verified by a set of markers including Bax, Bcl-2, cytosolic cytochrome c and caspase-3 up-regulation expression. Doxorubicin 20-31 BCL2-associated X protein Mus musculus 81-84 24748476-7 2014 The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1. Doxorubicin 90-93 BCL2-associated X protein Mus musculus 262-265 25680506-4 2015 The hepatic expression of Bax and Fas, representative intrinsic and extrinsic apoptotic molecules, respectively, was significantly increased by dosing with DOX. Doxorubicin 156-159 BCL2-associated X protein Mus musculus 26-29 24748476-7 2014 The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1. Doxorubicin 195-198 BCL2-associated X protein Mus musculus 262-265 26149967-4 2015 MCD sensitizes MCF-7 and Hepa1-6 cells to DOX, Combination of MCD and marginal dose of DOX reduces the cell viability, and promoted apoptosis through induction of pro-apoptotic protein, Bax, activation of caspase-8 and caspase-7, down regulation of anti-apoptotic protein Bcl-2 and finally promoting PARP cleavage. Doxorubicin 87-90 BCL2-associated X protein Mus musculus 186-189 25337186-8 2014 The caspase-3 activity of PLLA-DOX/pDA group was the highest using biochemical techniques, and the Bax: Bcl-2 ratio increased significantly in PLLA-DOX/pDA group through qRT-PCR analysis. Doxorubicin 148-151 BCL2-associated X protein Mus musculus 99-102 24581239-8 2014 RESULTS: The elevation of apoptotic DNA fragmentation and number of TUNEL-positive nuclei were accompanied with the upregulation of Bax in muscle after exposure to doxorubicin, but all these changes were neither seen in the muscle treated with acylated ghrelin nor unacylated ghrelin after doxorubicin exposure. Doxorubicin 164-175 BCL2-associated X protein Mus musculus 132-135 19890356-6 2009 Further studies showed that THSG inhibited reactive oxygen species (ROS) generation and prevented DOX-induced loss of mitochondrial membrane potential, caspase-3 activation and upregulation of Bax protein expression. Doxorubicin 98-101 BCL2-associated X protein Mus musculus 193-196 22763982-7 2012 Moreover, DOX injection attenuated HO-1 expression and enzymatic activity as well as increased P53 expression, modulated Bcl-2/Bax expression and enhanced caspase 3 activity. Doxorubicin 10-13 BCL2-associated X protein Mus musculus 127-130 23300809-6 2012 Instead, the combination treatment of DOX plus PI103 activated Bax, the mitochondrial apoptosis pathway, and caspase 3. Doxorubicin 38-41 BCL2-associated X protein Mus musculus 63-66 20655905-7 2010 Both mitochondrion-dependent and endoplasmic reticulum stress-induced apoptotic pathways were also activated in the hearts of doxorubicin-treated mice as reflected by decreased Bcl-2/Bcl-(XL) and elevated Bax/Bad, p53/Apaf-1, endoplasmic reticulum glucose-related protein 78, C/EBP homologous protein, cytochrome c release from mitochondria, caspases-9/-3 cleavage, and cardiomyocyte apoptosis. Doxorubicin 126-137 BCL2-associated X protein Mus musculus 205-208 20363884-9 2010 Further studies indicated that the Dox-induced higher levels of Hsp25 transactivated p53 leading to higher levels of the pro-apoptotic protein Bax, but other p53-related proteins remained unaltered. Doxorubicin 35-38 BCL2-associated X protein Mus musculus 143-146 20363884-11 2010 From these results we propose a novel mechanism for Dox-induced heart failure: increased expression of Hsp25 because of oxidant-induced activation of HSF-1 transactivates p53 to increase Bax levels, which leads to heart failure. Doxorubicin 52-55 BCL2-associated X protein Mus musculus 187-190 20074638-2 2010 Here we show that in adult mouse cardiomyocytes, DOX activates (i) the pro-apoptotic p53, (ii) p38MAPK and JNK, (iii) Bax translocation, (iv) cytochrome c release, and (v) caspase 3. Doxorubicin 49-52 BCL2-associated X protein Mus musculus 118-121 24326424-9 2014 Doxorubicin induced fibrosis (accumulated collagen deposition and increased CTGF), activated apoptosis (increased TUNEL index, apoptotic DNA fragmentation, and caspase-3 activity and decreased Bcl-2/Bax ratio), and suppressed phosphorylation status of prosurvival signals (ERK1/2 and Akt) in ventricular muscles. Doxorubicin 0-11 BCL2-associated X protein Mus musculus 199-202 21278141-8 2011 It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects. Doxorubicin 75-78 BCL2-associated X protein Mus musculus 196-199 21278141-8 2011 It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects. Doxorubicin 75-78 BCL2-associated X protein Mus musculus 227-230 21074598-7 2011 The levels of the pro-apoptotic proteins p53 and Bax and the anti-apoptotic protein Bcl-xL were significantly increased in Dox-treated mice compared with the control group. Doxorubicin 123-126 BCL2-associated X protein Mus musculus 49-52 18627295-6 2008 In DOX B1R(-/-) mice, cardiac dysfunction was improved compared to DOX control mice, which was associated with normalization of the bax/bcl-2 ratio and interleukin 6, as well as AKT activation state. Doxorubicin 3-6 BCL2-associated X protein Mus musculus 132-135 17718425-6 2007 Elevated expression of Bax was obviously observed after DOX treatment, while this elevation was prevented by MT induction by Zinc. Doxorubicin 56-59 BCL2-associated X protein Mus musculus 23-26 17718425-8 2007 CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio. Doxorubicin 128-131 BCL2-associated X protein Mus musculus 183-186 17718425-8 2007 CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio. Doxorubicin 128-131 BCL2-associated X protein Mus musculus 244-247 17718425-8 2007 CONCLUSION: These findings suggest that metallothionein induced by Zinc exhibits protective effects on the cardiac apoptosis of DOX, which might be mediated through the prevention of Bax protein up-regulation by DOX and associated elevation of Bax/Bcl-2 ratio. Doxorubicin 212-215 BCL2-associated X protein Mus musculus 183-186