PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30668372-10 2019 TQ pretreatment also inhibited As2O3-induced exacerbation in protein levels of BAX and PARP-1 and restored the loss of Bcl2 levels. Arsenic Trioxide 31-36 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 30600718-8 2018 The results showed lower cell viability rate, higher apoptosis ratio, higher BAX gene, and lower KI67 and BCL-2 genes" expression in cells exposed to MVs in combination with ATO compared to cells treated with each agent alone and non-treated control. Arsenic Trioxide 174-177 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 29959200-7 2018 When ATO is combined with Sorafenib, GSK3beta is activated, Mcl-1 is further reduced, and proapoptotic proteins Bak and Bax are activated. Arsenic Trioxide 5-8 BCL2 associated X, apoptosis regulator Homo sapiens 120-123 29164574-12 2017 CONCLUSIONS: As2O3 can inhibit proliferation of glioma cells and induce its apoptosis, which may be correlated with down-regulation of expressions of apoptosis-related factors, Fas, FasL and Bax, and apoptosis-related proteins, p53, caspase-3 and caspase-9. Arsenic Trioxide 13-18 BCL2 associated X, apoptosis regulator Homo sapiens 191-194 28823259-6 2017 CONCLUSION: Arsenic trioxide combined with itraconazole can inhibit the KG1a cell proliferation and induce apoptosis, which may be related with the inhibition of Hh signaling pathway and upregulation of both Caspase-3 and BAX protein expression, and provided experimental data of arsenic trioxide combined with itraconazole for the treatment of refractory AML. Arsenic Trioxide 12-28 BCL2 associated X, apoptosis regulator Homo sapiens 222-225 28239804-9 2017 RESULTS: Compared with normal control, As2O3 significantly increased BGC-823 cell apoptosis, blocked cell cycle in G0/G1 phase, elevated cAMP and Bax level, as well as downregulated PKC, Bcl-2 and Survivin expression (p < 0.05). Arsenic Trioxide 39-44 BCL2 associated X, apoptosis regulator Homo sapiens 146-149 27812249-5 2016 Additionally, combination of 2.5 mumol/L DAC and 5 mumol/L ATO led to a significantly higher apoptosis rate and more significantly decreased the Bcl2/Bax ratio than either compound alone (P < 0.001). Arsenic Trioxide 59-62 BCL2 associated X, apoptosis regulator Homo sapiens 150-153 28966729-12 2017 Western blot data showed that ATO upregulated the expression of caspase 3, Bax, and cytochrome C, and down-regulated the expression of Bcl-2. Arsenic Trioxide 30-33 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 27039805-4 2016 ATO further upregulated expression of Bax as an important proapoptotic target of NF-kappaB and also inhibited mRNA expression of survivin, c-Myc and hTERT and suppressed telomerase activity. Arsenic Trioxide 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 38-41 26883975-4 2016 KEY FINDINGS: Our results demonstrate that the nanoparticulate formulation of dimercaptosuccinic acid (DMSA) and chitosan coated As2O3 is capable of inducing morphological changes, DNA damage and caspase-dependent apoptosis along with the expression of cyclin-dependent kinase inhibitor p21 by upregulation of Bax and downregulation of Bcl-2 and Bcl-xL proteins. Arsenic Trioxide 129-134 BCL2 associated X, apoptosis regulator Homo sapiens 310-313 26607805-4 2016 Melatonin enhanced the ATO-induced apoptotic cell death via changes in the protein levels of Survivin, Bcl-2, and Bax, thus affecting cytochrome c release from the mitochondria to the cytosol. Arsenic Trioxide 23-26 BCL2 associated X, apoptosis regulator Homo sapiens 114-117 26117010-8 2015 Also, the expression of BCL-2 and survivin significantly decreased, while the expression of BAX, P21 and P27 was significantly upregulated in HL-60 cells after being treated with 5.0 micromol/L As2O3. Arsenic Trioxide 194-199 BCL2 associated X, apoptosis regulator Homo sapiens 92-95 25130820-9 2014 It is concluded that VPA can enhance the sensitivity of RPMI 8226 cells to ATO-induced apoptosis, which may be associated with decreasing the BCL-2 expression and increasing the BAX, caspase-8 and caspase-9 gene expression. Arsenic Trioxide 75-78 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 25416439-7 2015 ATO downregulated the expression of Bcl-2 and Bcl-xL and upregulated the expression of Bax, indicating that ATO could induce the apoptosis of HCC cells through the intrinsic pathways; but sorafenib showed little effects on these proteins of Bcl-2 family. Arsenic Trioxide 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 24993472-12 2015 CONCLUSIONS: As2O3 could restore the expression of TMS1 by inhibiting DNMT to reverse the hypermethylation and induced apoptosis of K562 cells by downregulation of Bcl-2/Bax expression. Arsenic Trioxide 13-18 BCL2 associated X, apoptosis regulator Homo sapiens 170-173 25174355-10 2014 Treatment with ATO resulted in phosphatidylserine externalization in H23 cells and mitochondrial membrane depolarization in all cell lines, associated with truncation of Bid, downregulation of Bcl-2, upregulation of Bax and Bak, caspase-9 and -3 activation and PARP cleavage. Arsenic Trioxide 15-18 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 25338570-9 2014 Arsenic trioxide combined with curcumin can effectively inhibit the KG1a cell proliferation and induce apoptosis, which may be associated with the downregulation of BCL-2 and PARP protein expression and the upregulation of BAX protein expression. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 223-226 25128771-8 2014 And, high dose of ATO increased Bax/Bcl-2 ratio in a time-dependent fashion and activated caspase-3 apoptotic signaling. Arsenic Trioxide 18-21 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 20403207-14 2010 Bax activation might also be involved in arsenic trioxide-induced Bcl-2 conformational change. Arsenic Trioxide 41-57 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 24944602-6 2014 In addition, ATO significantly decreased the expression of antiapoptotic proteins, B-cell lymphoma 2 (Bcl-2) and B cell lymphoma-extra large (Bcl-xL), but markedly increased the expression of proapoptotic proteins, including c-Jun N-terminal kinase (JNK), phosphorylated-JNK, Bax, full length caspase-3 and cleaved caspase-3. Arsenic Trioxide 13-16 BCL2 associated X, apoptosis regulator Homo sapiens 276-279 24944602-7 2014 These results indicated that ATO inhibited the proliferation and induced apoptosis in THP1 cells partially via blocking the inhibitory effects of EVI-1 on the JNK signaling pathway with the involvement of apoptosis-associated proteins, including Bax, Bcl-2, Bcl-xL and caspase-3. Arsenic Trioxide 29-32 BCL2 associated X, apoptosis regulator Homo sapiens 246-249 24666483-10 2014 CONCLUSION: As2O3 could up-regulate TMS1 gene expression by reversing its hypermethylation and induced apoptosis by down-regulation of Bcl-2/Bax ratio in K562 cells. Arsenic Trioxide 12-17 BCL2 associated X, apoptosis regulator Homo sapiens 141-144 23041229-3 2012 Using ATO and HL60 as drug and cell models, respectively, we observed that 2-DG/ATO combination activates the mitochondrial apoptotic pathway, as indicated by Bid-, and Bax-regulated cytochrome c and Omi/HtrA2 release, XIAP down-regulation, and caspase-9/-3 pathway activation. Arsenic Trioxide 80-83 BCL2 associated X, apoptosis regulator Homo sapiens 169-172 20605902-4 2010 Curcumin plus ATO or lonidamine stimulates typical events of the mitochondrial executioner pathway (Bax and Bid activation, cytochrome c release, X-linked inhibitor of apoptosis down-regulation, and caspase-9/-3 activation) and causes mitochondrial transmembrane potential dissipation, which nevertheless represents a late event in the apoptotic response. Arsenic Trioxide 14-17 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 20164150-0 2010 The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide. Arsenic Trioxide 133-149 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 24738333-12 2014 Moreover, transcription and protein expression of bcl-2, NFKB, survivin, bax, p53 and caspase-3 of Raji cells were regulated at the most remarkable extent in ADM-As2O3, MNPs group as compared with other groups. Arsenic Trioxide 162-167 BCL2 associated X, apoptosis regulator Homo sapiens 73-76 24466103-3 2014 Here we show that ATO dose-dependently induces depolarization of mitochondrial inner transmembrane potential (DeltaPsim), up-regulation of Bax and down-regulation of Bcl-2 and Bcl-XL, caspase-3 activation, and phosphotidylserine (PS) exposure in platelets. Arsenic Trioxide 18-21 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 24356076-7 2013 The expression of caspase-3 and Bax, which are targets of let-7d and miR-766, respectively, were up-regulated in As2O3 treated cells. Arsenic Trioxide 113-118 BCL2 associated X, apoptosis regulator Homo sapiens 32-35 22922982-12 2012 Since expression of Bax was unchanged following treatment, As2O3 effectively reduced the Bcl-2/Bax ratio. Arsenic Trioxide 59-64 BCL2 associated X, apoptosis regulator Homo sapiens 95-98 22922982-13 2012 As2O3 (1-2 microM) enhances the cytotoxic effects of 89SrCl2 on the MCF-7 human breast cancer cell line by inducing G2 phase delay and promoting apoptosis through the reduction of the Bcl-2/Bax ratio. Arsenic Trioxide 0-5 BCL2 associated X, apoptosis regulator Homo sapiens 190-193 20403207-15 2010 Arsenic trioxide did not change levels of total Bcl-2 expression, but up-regulated total Bax expression for the treatment time ranging from 3 to 24 hours. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 20403207-16 2010 CONCLUSION: Arsenic trioxide induces apoptosis through induction of Bcl-2 conformational change, Bax activation and up-regulation of total Bax expression rather than affecting total Bcl-2 expression in human gastric cancer SGC7901 cells. Arsenic Trioxide 12-28 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 20403207-16 2010 CONCLUSION: Arsenic trioxide induces apoptosis through induction of Bcl-2 conformational change, Bax activation and up-regulation of total Bax expression rather than affecting total Bcl-2 expression in human gastric cancer SGC7901 cells. Arsenic Trioxide 12-28 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 21061466-9 2010 ATO also significantly enhanced expression of Bax and cytochrome c proteins but suppressed those of Bcl-2. Arsenic Trioxide 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 17404572-0 2007 Arsenic trioxide-induced neuroblastoma cell death is accompanied by proteolytic activation of nuclear Bax. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 102-105 19489279-14 2009 Western blotting showed that the Bcl-2 expression was decreased and the expression of Bax increased after treatment of arsenic trioxide. Arsenic Trioxide 119-135 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 18412143-9 2008 In addition, N-acetyl-L-cystein (NAC), a thiol-containing anti-oxidant, completely blocked As2O3-induced p38 MAPK and JNK activations, mitochondria translocation of Bax, and phosphorylation of Bcl-2. Arsenic Trioxide 91-96 BCL2 associated X, apoptosis regulator Homo sapiens 165-168 18412143-10 2008 These results support a notion that ROS-mediated activations of p38 MAPK and JNK in response to As2O3 treatment signals activation of Bax and phosphorylation of Bcl-2, resulting in mitochondrial apoptotic cell death in human cervical cancer cells. Arsenic Trioxide 96-101 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 18695917-9 2008 These results indicate that activation of p38 MAPK is specifically required for translocation of Bax to the mitochondria, and both JNK and p38 MAPK are involved in phosphorylation of Bcl-2 in response to combination treatment with gamma-radiation and As2O3, and that ROS is a critical regulator of p38 MAPK and JNK activations. Arsenic Trioxide 251-256 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 18599993-4 2008 The activation of caspase-3 was increased, and the rate of bcl-2/bax was down-regulated in the HXO-RB(44) cells processed with arsenic trioxide. Arsenic Trioxide 127-143 BCL2 associated X, apoptosis regulator Homo sapiens 65-68 18359480-3 2008 Co-treatment with ATO plus quercetin caused mitochondrial transmembrane potential dissipation, stimulated the mitochondrial apoptotic pathway, as indicated by cytochrome c and Omi/Htra2 release, XIAP and Bcl-X(L) down-regulation, and Bax activation, and caused caspase-8/Bid activation. Arsenic Trioxide 18-21 BCL2 associated X, apoptosis regulator Homo sapiens 234-237 17673311-7 2007 P38-MAPK-specific inhibitors attenuate the As(2)O(3) plus TNFalpha-provoked activation of caspase-8/Bid, Bax translocation, cytochrome c release, and apoptosis induction. Arsenic Trioxide 43-52 BCL2 associated X, apoptosis regulator Homo sapiens 105-108 19664237-14 2009 Western blotting revealed that the expression of cell cycle related protein p21 and cyclin D1 were not affected by the treatments, whereas apoptosis related protein bax, Bcl-2, and clusterin were significantly regulated by As2O3 and/or DDP treatments compared with controls. Arsenic Trioxide 223-228 BCL2 associated X, apoptosis regulator Homo sapiens 165-168 18412143-3 2008 As2O3-induced apoptotic cell death in HeLa cells was associated with activation and mitochondrial translocation of Bax, a marked phosphorylation of Bcl-2, reduction of Bcl-2 and Bax interaction, dissipation of mitochondrial membrane potential. Arsenic Trioxide 0-5 BCL2 associated X, apoptosis regulator Homo sapiens 115-118 18412143-3 2008 As2O3-induced apoptotic cell death in HeLa cells was associated with activation and mitochondrial translocation of Bax, a marked phosphorylation of Bcl-2, reduction of Bcl-2 and Bax interaction, dissipation of mitochondrial membrane potential. Arsenic Trioxide 0-5 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 18412143-4 2008 Using small interfering RNA, reduced Bax expression effectively attenuated As2O3-induced mitochondrial membrane potential loss and apoptotic cell death. Arsenic Trioxide 75-80 BCL2 associated X, apoptosis regulator Homo sapiens 37-40 18412143-5 2008 Moreover, the phosphorylation of Bcl-2 induced by As2O3 diminished its ability to bind to Bax. Arsenic Trioxide 50-55 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 17404572-8 2007 The inability of overexpressed p18 Bax to locate to the nucleus, and the As(2)O(3)-induced reduction of p21 Bax in the cytosol, suggest an As(2)O(3)-induced mechanism where p18 Bax gets cleaved and "trapped" in the nucleus. Arsenic Trioxide 73-82 BCL2 associated X, apoptosis regulator Homo sapiens 108-111 17404572-8 2007 The inability of overexpressed p18 Bax to locate to the nucleus, and the As(2)O(3)-induced reduction of p21 Bax in the cytosol, suggest an As(2)O(3)-induced mechanism where p18 Bax gets cleaved and "trapped" in the nucleus. Arsenic Trioxide 73-82 BCL2 associated X, apoptosis regulator Homo sapiens 108-111 17203211-0 2007 Arsenic trioxide induces apoptosis via the mitochondrial pathway by upregulating the expression of Bax and Bim in human B cells. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 99-102 17390014-8 2007 However, the apoptosis-related proteins such as p21 and Bax were overexpressed by As4O6. Arsenic Trioxide 82-87 BCL2 associated X, apoptosis regulator Homo sapiens 56-59 16882451-8 2007 In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells. Arsenic Trioxide 39-44 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 16882451-8 2007 In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells. Arsenic Trioxide 39-44 BCL2 associated X, apoptosis regulator Homo sapiens 118-121 16882451-8 2007 In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells. Arsenic Trioxide 206-211 BCL2 associated X, apoptosis regulator Homo sapiens 118-121 17203211-4 2007 As2O3-induced apoptosis is associated with reduced mitochondrial transmembrane potential (delta psi), enhanced generation of intracellular reactive oxygen species (ROS), release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria into cytoplasm, activation of caspases, and upregulation of Bax and Bim expression. Arsenic Trioxide 0-5 BCL2 associated X, apoptosis regulator Homo sapiens 308-311 17237268-9 2007 These results indicate that phytosphingosine in combination with As(2)O(3) induces synergistic apoptosis in As(2)O(3)-resistant leukemia cells through the p38 MAPK-mediated mitochondrial translocation of Bax and the PARP-1 activation, and that p38 MAPK and PARP-1 activations are reactive oxygen species dependent. Arsenic Trioxide 108-117 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 17237268-9 2007 These results indicate that phytosphingosine in combination with As(2)O(3) induces synergistic apoptosis in As(2)O(3)-resistant leukemia cells through the p38 MAPK-mediated mitochondrial translocation of Bax and the PARP-1 activation, and that p38 MAPK and PARP-1 activations are reactive oxygen species dependent. Arsenic Trioxide 65-74 BCL2 associated X, apoptosis regulator Homo sapiens 204-207 15665116-4 2005 The potentiation of As2O3-provoked apoptosis involved the increased disruption of mitochondrial transmembrane potential, increased caspase-3 activation and cytochrome c release from mitochondria, increased Bax and Bid activation, and attenuation of 27-kDa heat shock protein (HSP27) expression; the potentiation was prevented by Bcl-2 overexpression. Arsenic Trioxide 20-25 BCL2 associated X, apoptosis regulator Homo sapiens 206-209 16010437-5 2005 ATO activated the intrinsic (mitochondrial) pathway of apoptosis, which involved disrupting mitochondrial membrane potential, increased Bax/Bcl-2 ratio and caspase-9 activation, as well as the extrinsic (death receptor) pathway mediated by Fas and caspase-8 activation. Arsenic Trioxide 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 136-139 11135700-3 2000 RESULTS: Arsenic trioxide could strongly inhibit the growth of human hepatocarcinoma cells QGY-7701 and QGY-7703 with the cell cycle arrested on S phase, and induce the apoptosis of the cells with bcl-2 gene expression down-regulated and bax and Fas gene expression up-regulated. Arsenic Trioxide 9-25 BCL2 associated X, apoptosis regulator Homo sapiens 238-241 15131059-0 2004 Arsenic trioxide-induced death of neuroblastoma cells involves activation of Bax and does not require p53. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 15735709-0 2005 Arsenic trioxide (As(2)O(3)) induces apoptosis through activation of Bax in hematopoietic cells. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 15735709-1 2005 This study explores the roles of Bax and other Bcl-2 family members play in arsenic trioxide (As(2)O(3))-induced apoptosis. Arsenic Trioxide 76-92 BCL2 associated X, apoptosis regulator Homo sapiens 33-36 15735709-5 2005 Meanwhile, Bax conformational change and oligomerization induced by As(2)O(3) were not inhibited by the pancaspase inhibitor z-VAD-fmk, although Bid cleavage could be completely abolished. Arsenic Trioxide 68-77 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 11819674-11 2000 The induced-apoptosis effect of 1,2&mgr;mol/L arsenic trioxide was related to the expression level of Bcl-2 and Bax. Arsenic Trioxide 50-66 BCL2 associated X, apoptosis regulator Homo sapiens 116-119 11819674-4 2000 Flow cytometry was used to assay cell-DNA distribution and the protein expression of Bcl-2 and Bax detected by immunocytochemical method.RESULTS:The cell growth was significantly inhibited by varying concentrations of arsenic trioxide as revealed by cell counting and cell-growth curve, which was dose- and time-dependent. Arsenic Trioxide 218-234 BCL2 associated X, apoptosis regulator Homo sapiens 95-98 11819674-9 2000 High expressions of Bcl-2 and Bax were detected in 1 and 2&mgr;mol/L arsenic trioxide-treated cells, these were 46%, 87.33% and 83.08%, 95.83% respectively, among which that of Bax was more significant. Arsenic Trioxide 73-89 BCL2 associated X, apoptosis regulator Homo sapiens 30-33 11819674-9 2000 High expressions of Bcl-2 and Bax were detected in 1 and 2&mgr;mol/L arsenic trioxide-treated cells, these were 46%, 87.33% and 83.08%, 95.83% respectively, among which that of Bax was more significant. Arsenic Trioxide 73-89 BCL2 associated X, apoptosis regulator Homo sapiens 181-184 11819674-10 2000 Arsenic trioxide treatment at 0.5&mgr;mol/L resulted in a higher expression level of Bcl-2 and lower expression level of Bax,which were 8.81% and 3.83% respectively, as compared with that of the control group (15.33%) (P(1)<0.01, P(2)<0.01).CONCLUSION:Arsenic trioxide not only inhibited proliferation but also induced apoptosis of human hepatoma cell line BEL-7402. Arsenic Trioxide 0-16 BCL2 associated X, apoptosis regulator Homo sapiens 125-128 15622746-5 1997 Furthermore, As2O3 effectively down-regulated the expression of bcl-2 gene without changing the mRNA levels of other apoptosis-associated genes (including p53, c-myc, bax and bcl-XL). Arsenic Trioxide 13-18 BCL2 associated X, apoptosis regulator Homo sapiens 167-170 31079498-8 2019 Overexpression of Id-1 could attenuate the inhibition or promotion of As2O3 on proliferation, apoptosis and Caspase-3, Bax and Bcl-2 protein expression in Tca8113 cells. Arsenic Trioxide 70-75 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 34659521-5 2021 Both Met and ATO effectively inhibited the proliferative activity of HeLa cells and induced apoptosis by activating Bax and inhibiting Bcl-2. Arsenic Trioxide 13-16 BCL2 associated X, apoptosis regulator Homo sapiens 116-119 35487055-9 2022 Generally, both cell lines treated with the combination of Curcumin and As2O3 displayed decreased angiogenesis genes (VEGFA and VEGFC), apoptosis genes (BAX and Bcl2), and prostate cancer marker (KLK2), the zinc-finger protein (SNAIL); and an increase in expression (P < 0.05) of cell-cell adhesion molecule (E-cadherin) and tumor suppressor gene (P53) genes. Arsenic Trioxide 72-77 BCL2 associated X, apoptosis regulator Homo sapiens 153-156 32642412-3 2020 In this study, we showed that high concentrations of As2O3 induced apoptosis of pDCs via mitochondrial pathway with increased BAX/BCL-2 ratio, while independent of reactive oxygen species generation. Arsenic Trioxide 53-58 BCL2 associated X, apoptosis regulator Homo sapiens 126-129