PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22142431-2 2012 EtOH-induced nuclear clusterin interacts with Bcl(XL), thereby liberating proapoptotic Bax. Ethanol 0-4 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 24961420-3 2013 The ethanol-induced apoptosis is mitochondria-dependent, involving Bax and caspase-3 activation. Ethanol 4-11 BCL2 associated X, apoptosis regulator Homo sapiens 67-70 12603597-8 2003 Ethanol decreased Jurkat cell expression of Bcl-2, whereas ethanol increased Jurkat cell expression of Bax. Ethanol 59-66 BCL2 associated X, apoptosis regulator Homo sapiens 103-106 22138516-9 2012 CONCLUSIONS: The study showed that major active component in the ethanol extract of Glycosmis pentaphylla is a flavonoid which induces apoptosis on cancer cell line, Hep3 B, by increasing the expression ratio of Bax/Bcl2 genes in a time and dose dependent manner. Ethanol 65-72 BCL2 associated X, apoptosis regulator Homo sapiens 212-215 21240456-8 2011 Our results suggest that p53 sensitizes tumor cells to the ethanol extract of Iris nertschinskia by Bax protein induction and caspase-dependent apoptosis. Ethanol 59-66 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 21348303-6 2010 Western blotting analysis revealed that in ethanol treated cells preconditioned with NaNO2, the HIF-1alpha and Bcl-2 increased obviously, while the expression of pro-apoptotic proteins, including Bax, Caspase-9, Caspase-3 decreased. Ethanol 43-50 BCL2 associated X, apoptosis regulator Homo sapiens 196-199 19382207-13 2009 Cells overexpressing WT or S9A GSK3beta were much more sensitive to ethanol-induced Bax activation than parental SK-N-MC cells. Ethanol 68-75 BCL2 associated X, apoptosis regulator Homo sapiens 84-87 15977640-4 2005 We have previously demonstrated that ethanol-induced neuron apoptosis is critically dependent on expression of Bax, a proapoptotic member of the Bcl-2 family. Ethanol 37-44 BCL2 associated X, apoptosis regulator Homo sapiens 111-114 15977640-6 2005 Ethanol produced extensive Bax-dependent caspase-3 activation and neuron apoptosis in the cerebellar internal granule cell layer, which was maximal at approximately 6 hours postadministration. Ethanol 0-7 BCL2 associated X, apoptosis regulator Homo sapiens 27-30 12748063-4 2003 This may be due, in part, to the increased propensity of the mitochondria in ethanol-exposed cells to induction of mitochondrial permeability transition (MPT) by various agents, including the proapoptotic protein Bax. Ethanol 77-84 BCL2 associated X, apoptosis regulator Homo sapiens 213-216 12748063-8 2003 Moreover, the ethanol-enhanced pathway is dependent on p38 MAPK signaling, which brings about caspase-3 activation, mitochondrial depolarization, accumulation of cytochrome c in the cytosol, and the translocation of Bax to the mitochondria. Ethanol 14-21 BCL2 associated X, apoptosis regulator Homo sapiens 216-219 12748063-9 2003 Additionally, ethanol-exposed cells display a blunting of TNF-alpha-induced Akt activation and Bcl-2 antagonist of cell death phosphorylation that may account, in part, for the increased sensitivity of the mitochondria to Bax-mediated damage. Ethanol 14-21 BCL2 associated X, apoptosis regulator Homo sapiens 222-225 21457722-0 2011 The ethanol extract of Scutellaria baicalensis and the active compounds induce cell cycle arrest and apoptosis including upregulation of p53 and Bax in human lung cancer cells. Ethanol 4-11 BCL2 associated X, apoptosis regulator Homo sapiens 145-148 19775596-13 2009 Ethanol also shifted the Bcl-2/Bax balance towards apoptosis. Ethanol 0-7 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 11791174-4 2002 Expression of both anti-apoptotic (such as Bcl-2 and Bcl-x(L)) and proapoptotic (such as Bax) proteins is markedly elevated in the liver of human ALD and chronically ethanol-fed IL-6 (+/+) mice. Ethanol 166-173 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 34066632-8 2021 The role of caspase-9 in hyperthermia treated cells acquired significance whether ethanol was present during hyperthermia since the alcohol enhanced Bid cleavage, translocation of Bax from cytosol to mitochondria, release of mitochondrial apoptogenic factors, and decreased of the levels of the anti-apoptotic factor myeloid cell leukemia-1 (Mcl-1). Ethanol 82-89 BCL2 associated X, apoptosis regulator Homo sapiens 180-183 11021353-9 2000 The content of Bax and the activities of Caspase 3 were increased upon ethanol exposure. Ethanol 71-78 BCL2 associated X, apoptosis regulator Homo sapiens 15-18 10951621-6 2000 CONCLUSION: The overexpression of Bax, Bak proteins may play a role in HepG(2) cell apoptosis induced by ethanol and can be blocked effectively by Bcl-2 adenovirus vector. Ethanol 105-112 BCL2 associated X, apoptosis regulator Homo sapiens 34-37 26677054-11 2016 The Bax/Bcl-2 ratio was dose-dependently decreased by EtOH and by high-dose EtP in A549 cells, indicating a reduction in apoptosis, whereas this effect was not observed in Huh7 cells. Ethanol 54-58 BCL2 associated X, apoptosis regulator Homo sapiens 4-7 30875026-11 2019 A curcumin nanoformulation sized 77 nm and containing of 3% ethanol was more effective in increasing beta1-integrin gene over-expression, anti-apoptosis of fibroblast cells (Bcl2/Bax ratio), and in decreasing Bax and NFkappaB gene expression than that with a particle size of 50 nm. Ethanol 60-67 BCL2 associated X, apoptosis regulator Homo sapiens 179-182 30875026-11 2019 A curcumin nanoformulation sized 77 nm and containing of 3% ethanol was more effective in increasing beta1-integrin gene over-expression, anti-apoptosis of fibroblast cells (Bcl2/Bax ratio), and in decreasing Bax and NFkappaB gene expression than that with a particle size of 50 nm. Ethanol 60-67 BCL2 associated X, apoptosis regulator Homo sapiens 209-212 28928657-7 2017 Our study in metastatic MDA-MB-231 cells showed that both ethanol and acetone pulp extracts decreased transcript levels of the anti-apoptotic genes BCL2 and BCLXL, and a reverse effect was observed for the pro-apoptotic genes BAX and caspase 3. Ethanol 58-65 BCL2 associated X, apoptosis regulator Homo sapiens 226-229 28081301-7 2017 RESULTS: EtOH dose dependently induces depolarization of mitochondrial inner transmembrane potential, up-regulation of Bax, down-regulation of Bcl-2, and caspase-3 activation. Ethanol 9-13 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 27854008-4 2017 Western blots revealed that ethanol preconditioning upregulated expression of the anti-apoptotic protein Bcl-2 and downregulated the pro-apoptotic protein Bax. Ethanol 28-35 BCL2 associated X, apoptosis regulator Homo sapiens 155-158 32774685-4 2020 Our data show that 200 mug/mL of ethanol extract of Tribulus terrestris (EE-TT) significantly increased the cell viability and prevented the apoptosis of H2O2-treated ARPE-19 cells through the regulation of Bcl2, Bax, cleaved caspase-3, and caspase-9. Ethanol 33-40 BCL2 associated X, apoptosis regulator Homo sapiens 213-216 28197783-17 2017 Western blotting analysis on the expression of apoptosis regulatory proteins showed enhancement of proteocleavage-activated caspases 3, 8, and 9 and higher ratios of Bax/Bcl2 in the liquid nitrogen- and freezing nitrogen ethanol composite-treated samples. Ethanol 221-228 BCL2 associated X, apoptosis regulator Homo sapiens 166-169 23688633-7 2013 In particular, the autophagic process induced by gAcrp was involved in the suppression of ethanol-induced activation of caspase-8 and expression of Bax. Ethanol 90-97 BCL2 associated X, apoptosis regulator Homo sapiens 148-151 25190223-10 2014 The 1% ethanol group showed significantly (P<0.05) higher mRNA expression levels of poly(ADP-ribose) polymerase-1 (PARP-1), Bax, Bak and caspase-3, and the 3% ethanol group had significantly (P<0.05) increased PARP-1, Bax and caspase-3 mRNA expression levels compared with the control group. Ethanol 7-14 BCL2 associated X, apoptosis regulator Homo sapiens 127-130 25190223-10 2014 The 1% ethanol group showed significantly (P<0.05) higher mRNA expression levels of poly(ADP-ribose) polymerase-1 (PARP-1), Bax, Bak and caspase-3, and the 3% ethanol group had significantly (P<0.05) increased PARP-1, Bax and caspase-3 mRNA expression levels compared with the control group. Ethanol 7-14 BCL2 associated X, apoptosis regulator Homo sapiens 224-227 25881894-9 2015 In the ethanol-treated cerebellar granule neurons we find an increased expression of genes related to apoptosis (Mapk8 and Bax), but also of genes previously described as neuroprotective (Dhcr24 and Bdnf), which might suggest an actively maintained viability. Ethanol 7-14 BCL2 associated X, apoptosis regulator Homo sapiens 123-126 25779081-6 2015 Interestingly, although ethanol induced mitochondrial Bax translocation, this episode was associated to cell death rather than mitochondrial fission or autophagy responses. Ethanol 24-31 BCL2 associated X, apoptosis regulator Homo sapiens 54-57 25779081-7 2015 Thus, Bax required 600 mM ethanol to migrate to mitochondria, a concentration that resulted in cell death. Ethanol 26-33 BCL2 associated X, apoptosis regulator Homo sapiens 6-9 24571090-10 2014 Western blot analysis demonstrated that EtOH and n-hexane extracts upregulated Bax expression, also it induced cleavage of PARP in HeLa cells compared to the control. Ethanol 40-44 BCL2 associated X, apoptosis regulator Homo sapiens 79-82