PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8619857-4 1996 Although Bcl-2 has been shown to act as an antioxidant under certain conditions, additional functions have emerged from studies under low oxygen pressure. Oxygen 138-144 BCL2 apoptosis regulator Homo sapiens 9-14 10360831-7 1999 We demonstrated that over-expression of bcl-2 inhibited LND-induced apoptosis, while reducing 14CO2 production, oxygen uptake and ATP content, whereas aerobic lactate production was essentially unaffected. Oxygen 112-118 BCL2 apoptosis regulator Homo sapiens 40-45 22358524-5 1997 We also present new data which demonstrates that bcl-2 can protect cells from apoptosis induced by oxygen deprivation, a finding which has important implications for large scale and intensive cultivation of cells. Oxygen 99-105 BCL2 apoptosis regulator Homo sapiens 49-54 9209397-2 1997 Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), we find that expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia) and that the cell death does not involve ROS, suggesting that Bcl-2 or Bcl-xL exerts an anti-cell death function by a mechanism other than through regulation of ROS activity. Oxygen 80-86 BCL2 apoptosis regulator Homo sapiens 53-58 9209397-2 1997 Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), we find that expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia) and that the cell death does not involve ROS, suggesting that Bcl-2 or Bcl-xL exerts an anti-cell death function by a mechanism other than through regulation of ROS activity. Oxygen 80-86 BCL2 apoptosis regulator Homo sapiens 129-134 9209397-2 1997 Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), we find that expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia) and that the cell death does not involve ROS, suggesting that Bcl-2 or Bcl-xL exerts an anti-cell death function by a mechanism other than through regulation of ROS activity. Oxygen 80-86 BCL2 apoptosis regulator Homo sapiens 129-134 7536895-0 1995 Programmed cell death and Bcl-2 protection in very low oxygen. Oxygen 55-61 BCL2 apoptosis regulator Homo sapiens 26-31 8551333-3 1996 Infection of hippocampal cultures with Bcl-2 vectors enhanced neuron survivorship after exposure to adriamycin, a potent oxygen radical generator. Oxygen 121-127 BCL2 apoptosis regulator Homo sapiens 39-44 7723826-3 1995 Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia), which drastically decreases the net formation of oxygen free radicals and does not increase oxidized lipid, protein or DNA. Oxygen 80-86 BCL2 apoptosis regulator Homo sapiens 53-58 7723826-3 1995 Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia), which drastically decreases the net formation of oxygen free radicals and does not increase oxidized lipid, protein or DNA. Oxygen 80-86 BCL2 apoptosis regulator Homo sapiens 116-121 35093886-4 2022 RESULTS: We observed an increase in O2 - production only in BCL2KO NB cells treated with cisplatin (three-fold) and CasIIIia (five-fold), whereas the production of H2O2 in BCL2KO NB cells treated with cisplatin and CasIIIia increased five-fold and three-fold, respectively. Oxygen 36-40 BCL2 apoptosis regulator Homo sapiens 60-64 7503812-2 1993 Bcl-2 is localized to intracellular sites of oxygen free radical generation including mitochondria, endoplasmic reticula, and nuclear membranes. Oxygen 45-51 BCL2 apoptosis regulator Homo sapiens 0-5 34302634-0 2021 Lactucin induces apoptosis through reactive oxygen species-mediated BCL-2 and CFLARL downregulation in Caki-1 cells. Oxygen 44-50 BCL2 apoptosis regulator Homo sapiens 68-73 21364630-7 2010 Western blotting revealed significantly upregulated oxygen-sensitive transcription factors hypoxia-inducible factor (HIF)-1alpha and HIF-2alpha, while producing a biphasic response within HIF targets, including erythropoietin, vascular endothelial growth factor and Bcl-2 family members, during hypoxia and subsequent reoxygenation. Oxygen 52-58 BCL2 apoptosis regulator Homo sapiens 266-271 34967955-4 2022 Then, TUNEL analysis showed that the 5% oxygen concentration group significantly inhibited apoptosis of cumulus-oocyte complexes (COCs) compared to the other group, and the transcription and protein levels of pro-apoptotic factor Bax, HIF-1alpha and VEGF in yak COCs significantly reduced, while anti-apoptotic factor Bcl-2 significantly increased. Oxygen 40-46 BCL2 apoptosis regulator Homo sapiens 318-323 35093886-4 2022 RESULTS: We observed an increase in O2 - production only in BCL2KO NB cells treated with cisplatin (three-fold) and CasIIIia (five-fold), whereas the production of H2O2 in BCL2KO NB cells treated with cisplatin and CasIIIia increased five-fold and three-fold, respectively. Oxygen 36-40 BCL2 apoptosis regulator Homo sapiens 172-176 30015875-6 2018 Secondly, the stable overexpression of Bcl-2 and ability to shift metabolism towards oxidative phosphorylation (OXPHOS) in SKOV3/DDP cells were associated with increased oxygen consumption. Oxygen 170-176 BCL2 apoptosis regulator Homo sapiens 39-44 32562827-6 2020 The current results showed that the apoptosis in porcine GCs exposed to severe hypoxia (1% O2) was correlated with enhanced activation of c-Jun N-terminal kinase (JNK), nuclear accumulation of FOXO1, as well as elevated level of cleaved caspase-3 and decreased ratio of BCL-2/BAX. Oxygen 91-93 BCL2 apoptosis regulator Homo sapiens 270-275 31727766-0 2020 CD34+ acute myeloid leukemia cells with low levels of reactive oxygen species show increased expression of stemness-genes and can be targeted by the BCL2 inhibitor Venetoclax. Oxygen 63-69 BCL2 apoptosis regulator Homo sapiens 149-153 29665051-5 2018 Mechanistic studies revealed that the sensitizing effect of hyperbaric oxygen is due to decreased ratio of Bcl-2/Bax, increased level of p53, cleaved Caspase3, GRP78, CHOP, and LC3. Oxygen 71-77 BCL2 apoptosis regulator Homo sapiens 107-112 26173295-0 2015 Upregulation of Bcl-2 enhances secretion of growth factors by adipose-derived stem cells deprived of oxygen and glucose. Oxygen 103-109 BCL2 apoptosis regulator Homo sapiens 16-21 25519716-6 2015 In addition, the ratio of BAX/BCL2 also increased after adding vitamin C under conditions of 2% O2, while the gene expression level of BCL2 increased after adding vitamin C under increasing oxygen concentrations. Oxygen 96-98 BCL2 apoptosis regulator Homo sapiens 30-34 25519716-6 2015 In addition, the ratio of BAX/BCL2 also increased after adding vitamin C under conditions of 2% O2, while the gene expression level of BCL2 increased after adding vitamin C under increasing oxygen concentrations. Oxygen 190-196 BCL2 apoptosis regulator Homo sapiens 135-139 26173295-9 2015 In addition, Bcl-2 overexpression enhanced the secretion of VEGF, bFGF, and HGF by 14.47%, 16.9%, and 91%, respectively, compared to ADSCs alone that were deprived of oxygen and glucose. Oxygen 167-173 BCL2 apoptosis regulator Homo sapiens 13-18 26173295-10 2015 These data suggest that Bcl-2 overexpression enhances secretion of angiogenic growth factors by ADSCs deprived of oxygen and glucose. Oxygen 114-120 BCL2 apoptosis regulator Homo sapiens 24-29 23165748-9 2013 In conclusion, TSA inhibited the growth of HeLa cells via Bcl-2-mediated apoptosis, which was closely related to O2 - and GSH content levels. Oxygen 137-139 BCL2 apoptosis regulator Homo sapiens 70-75 24001324-10 2013 Oxygen pretreatment inhibited caspase 3 activation and decreased Bax/Bcl-2 ratio. Oxygen 0-6 BCL2 apoptosis regulator Homo sapiens 69-74 21967640-6 2012 In response to stress signals, traffic of pro- and antiapoptotic mitochondrial proteins in the intermembrane space (B-cell lymphoma-extra large, Bcl-2-associated death promoter, Bcl-2 associated X-protein and cytochrome c) is modulated by the redox condition determined by mitochondrial O2 utilization and mitochondrial nitric oxide metabolism. Oxygen 287-289 BCL2 apoptosis regulator Homo sapiens 145-150 21967640-6 2012 In response to stress signals, traffic of pro- and antiapoptotic mitochondrial proteins in the intermembrane space (B-cell lymphoma-extra large, Bcl-2-associated death promoter, Bcl-2 associated X-protein and cytochrome c) is modulated by the redox condition determined by mitochondrial O2 utilization and mitochondrial nitric oxide metabolism. Oxygen 287-289 BCL2 apoptosis regulator Homo sapiens 178-183 20668552-7 2010 The bcl-2-induced HIF-1alpha stabilization in response to low oxygen tension conditions was achieved through the impairment of ubiquitin-dependent HIF-1alpha degradation involving the molecular chaperone HSP90, but it was not dependent on the prolyl hydroxylation of HIF-1alpha protein. Oxygen 62-68 BCL2 apoptosis regulator Homo sapiens 4-9 21486225-7 2011 Overexpression of Bcl-2 increases mitochondrial oxygen consumption and in doing so generates a slight pro-oxidant intracellular milieu, which promotes genomic instability and blocks death signalling. Oxygen 48-54 BCL2 apoptosis regulator Homo sapiens 18-23 21265562-6 2011 Docking of heme onto a high-resolution structure of the G-quadruplex fold of Bcl-2 promoter DNA, which both binds heme and transfers oxygen, suggests a relatively open active site for this class of ribozymes and deoxyribozymes. Oxygen 133-139 BCL2 apoptosis regulator Homo sapiens 77-82 20367277-4 2010 Whereas overexpression of Bcl-2 increased mitochondrial oxygen consumption and complex IV activity, CEM/Bcl-2 cells responded to the increased mitochondrial oxidative stress induced by resveratrol by significantly reducing mitochondrial respiration, complex IV activity, and O(2)(-) production, and promoted cell survival. Oxygen 56-62 BCL2 apoptosis regulator Homo sapiens 26-31 19366737-3 2009 Using pharmacological and immunochemical methods, we tested the role of mitochondrial permeability transition (MPT) and the Bcl-2 proteins in oxygen-dependent radiosensitivity. Oxygen 142-148 BCL2 apoptosis regulator Homo sapiens 124-129 19580395-2 2009 The BCL-2 family of proteins regulate cell death in response to anoxia (0-0.5% O2). Oxygen 79-81 BCL2 apoptosis regulator Homo sapiens 4-9 19580395-4 2009 In this review, we discuss how mitochondria, BCL-2 proteins, and HIFs are crucial for cellular responses to low oxygen. Oxygen 112-118 BCL2 apoptosis regulator Homo sapiens 45-50 19366737-7 2009 Nor was evidence found for the modulation of oxygen-dependent radiosensitivity by Bax/Bcl-2 signalling, mitochondrial ATP-dependent potassium (mitoK(ATP)) channels or mitochondrial Ca(2+) uptake. Oxygen 45-51 BCL2 apoptosis regulator Homo sapiens 86-91 19298750-6 2009 CONCLUSION: On a molecular level, hyperbaric oxygen therapy leads to activation of ion channels, inhibition of hypoxia inducible factor-1alpha, up-regulation of Bcl-2, inhibition of MMP-9, decreased cyclooxygenase-2 activity, decreased myeloperoxidase activity, up-regulation of superoxide dismutase and inhibition of Nogo-A (an endogenous growth-inhibitory factor). Oxygen 45-51 BCL2 apoptosis regulator Homo sapiens 161-166 10657030-0 2000 Bcl-2 overexpression attenuates dopamine-induced apoptosis in an immortalized neural cell line by suppressing the production of reactive oxygen species. Oxygen 137-143 BCL2 apoptosis regulator Homo sapiens 0-5 19095301-5 2009 We have recently reported on the expression and function of two Bcl-2 family members in normal placental development, namely the pro-apoptotic Mtd/Bok, and its anti-apoptotic partner Mcl-1 and have found that their expression is upregulated by low oxygen, a key mediator of trophoblast cell proliferation in early placentation. Oxygen 248-254 BCL2 apoptosis regulator Homo sapiens 64-69 17510660-5 2007 We report a higher level of COX activity, oxygen consumption and mitochondrial respiration in tumor cells overexpressing Bcl-2. Oxygen 42-48 BCL2 apoptosis regulator Homo sapiens 121-126 16103078-4 2005 We found that 24-hour hypoxia (<0.1% O2) alone (no serum deprivation) showed sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) associated with bcl-2 up-regulation and resistance to etoposide-induced (5 mumol/L) apoptosis. Oxygen 40-42 BCL2 apoptosis regulator Homo sapiens 171-176 11236678-0 2000 [Effect of hyperbaric oxygen on the expression of proteins Bcl-2 and Bax in the gerbil hippocampus CA1 following forebrain ischemia reperfusion]. Oxygen 22-28 BCL2 apoptosis regulator Homo sapiens 59-64 19052874-11 2009 Regulation of Fas and Bcl-2 may be regarded as protective measures of the cell in response to hyperbaric oxygen. Oxygen 105-111 BCL2 apoptosis regulator Homo sapiens 22-27 17989353-3 2008 Here we show that treatment of neuronal cell line (SHSY-5Y) with antisense ORNs targeting the bcl-2 ARE (bcl-2 ARE asORNs) prevents bcl-2 down-regulation in response to apoptotic stimuli with glucose/growth factor starvation (Locke medium) or oxygen deprivation and enhances the apoptotic threshold as evaluated by time-lapse videomicroscopy, fluorescence-activated cell sorting analysis, and caspase-3 activation. Oxygen 243-249 BCL2 apoptosis regulator Homo sapiens 94-99 17989353-3 2008 Here we show that treatment of neuronal cell line (SHSY-5Y) with antisense ORNs targeting the bcl-2 ARE (bcl-2 ARE asORNs) prevents bcl-2 down-regulation in response to apoptotic stimuli with glucose/growth factor starvation (Locke medium) or oxygen deprivation and enhances the apoptotic threshold as evaluated by time-lapse videomicroscopy, fluorescence-activated cell sorting analysis, and caspase-3 activation. Oxygen 243-249 BCL2 apoptosis regulator Homo sapiens 105-110 17989353-3 2008 Here we show that treatment of neuronal cell line (SHSY-5Y) with antisense ORNs targeting the bcl-2 ARE (bcl-2 ARE asORNs) prevents bcl-2 down-regulation in response to apoptotic stimuli with glucose/growth factor starvation (Locke medium) or oxygen deprivation and enhances the apoptotic threshold as evaluated by time-lapse videomicroscopy, fluorescence-activated cell sorting analysis, and caspase-3 activation. Oxygen 243-249 BCL2 apoptosis regulator Homo sapiens 105-110 15013368-9 2004 VEGF and Bcl-2 immunoreactivity increased with prolonged exposure and increased extent of oxygen/metabolite deprivation. Oxygen 90-96 BCL2 apoptosis regulator Homo sapiens 9-14 12370489-5 2002 Pro-apoptotic Bcl-2 family members such as bax or bak are clearly required to initiate cytochrome c/apaf-1/caspase-9 mediated cell death during oxygen deprivation. Oxygen 144-150 BCL2 apoptosis regulator Homo sapiens 14-19 12370489-6 2002 Here we review what is currently known oxygen deprivation induced cell death and speculate about initiating mechanisms resulting in the activation of pro-apoptotic Bcl-2 family members. Oxygen 39-45 BCL2 apoptosis regulator Homo sapiens 164-169 11865975-2 2001 Furthermore, it has been proposed that BCL-2 acts to inhibit cell death by interfering with the production of oxygen-derived free radicals induced by a wide variety of stimuli. Oxygen 110-116 BCL2 apoptosis regulator Homo sapiens 39-44