PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23921841-8 2013 The apoptosis-promoting effect of licochalcone A may be mediated by its stimulatory action on the formation of reactive oxygen species and the depletion of GSH, which results in the activation of caspases. Glutathione 156-159 caspase 8 Homo sapiens 196-204 21113647-7 2011 The number of glutathione (GSH)-depleted cells was increased in 150 muM BHA-treated cells, which was attenuated by caspase inhibitors. Glutathione 14-25 caspase 8 Homo sapiens 115-122 21399877-8 2011 Caspase-8 and -9 inhibitors increased the number of GSH-depleted cells in MG132-treated HPF cells. Glutathione 52-55 caspase 8 Homo sapiens 0-16 21113647-7 2011 The number of glutathione (GSH)-depleted cells was increased in 150 muM BHA-treated cells, which was attenuated by caspase inhibitors. Glutathione 27-30 caspase 8 Homo sapiens 115-122 21113647-8 2011 In conclusion, BHA inhibited the growth of HeLa cells via caspase-dependent apoptosis, which seemed to be related to increase in GSH depletion and O(2)( -) level. Glutathione 129-132 caspase 8 Homo sapiens 58-65 15276073-2 2004 Viability loss and decrease in GSH contents in small cell lung cancer (SCLC) cells treated with MG132 was attenuated by caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk). Glutathione 31-34 caspase 8 Homo sapiens 120-127 19496190-7 2009 Additionally, ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity. Glutathione 116-119 caspase 8 Homo sapiens 156-165 17567462-2 2007 The antioxidant glutathione (GSH) regulates cell death pathways by modulating the redox state of specific thiol residues of target proteins including transcription factors, stress kinases and caspases, which participate in tumor necrosis factor (TNF)-induced apoptosis. Glutathione 16-27 caspase 8 Homo sapiens 192-200 17567462-2 2007 The antioxidant glutathione (GSH) regulates cell death pathways by modulating the redox state of specific thiol residues of target proteins including transcription factors, stress kinases and caspases, which participate in tumor necrosis factor (TNF)-induced apoptosis. Glutathione 29-32 caspase 8 Homo sapiens 192-200 17567462-5 2007 Cytosol GSH regulates TNF hepatocyte apoptosis by modulating caspase 8 activation or NF-kappaB-dependent gene expression. Glutathione 8-11 caspase 8 Homo sapiens 61-70 17222828-0 2007 GSH-dependent regulation of Fas-mediated caspase-8 activation by acrolein. Glutathione 0-3 caspase 8 Homo sapiens 41-50 17222828-1 2007 Activation of the cysteine protease caspase-8 by the death receptor Fas (CD95/APO-1) in B lymphoblastoid SKW6.4 cells or Jurkat T cells is associated with GSH depletion. Glutathione 155-158 caspase 8 Homo sapiens 36-45 17222828-2 2007 Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation. Glutathione 12-15 caspase 8 Homo sapiens 111-120 17222828-2 2007 Conversely, GSH depletion by the aldehyde acrolein (3-30 microM) was associated with inhibition of Fas-induced caspase-8 activation, although GSH depletion by buthionine sulfoximine (BSO) did not affect caspase-8 activation. Glutathione 12-15 caspase 8 Homo sapiens 203-212 15450951-3 2004 The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO). Glutathione 47-50 caspase 8 Homo sapiens 92-99 18304628-3 2008 Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts. Glutathione 100-103 caspase 8 Homo sapiens 182-202 18304628-3 2008 Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts. Glutathione 100-103 caspase 8 Homo sapiens 182-189 18304628-3 2008 Biochemical studies showed that CDDO-Im: induced a rapid and marked GSH depletion and antioxidants (GSH or NAC) completely inhibited its pro-apoptotic effect; sequentially activated caspase-8, -9 and -3; caspase inhibitors partially protected AML blasts from CDDO-Im-induced apoptosis; resistance of AML blasts to CDDO-Im-induced apoptosis correlated with low caspase-8/FADD and high Bcl-X(L) expression in leukemic blasts. Glutathione 100-103 caspase 8 Homo sapiens 182-191 17554377-5 2007 This internalization was closely relevant to intracellular glutathione (GSH) depletion in Jurkat cells downstream of Fas-associated death domain protein (FADD) and caspase 8. Glutathione 59-70 caspase 8 Homo sapiens 164-173 17554377-5 2007 This internalization was closely relevant to intracellular glutathione (GSH) depletion in Jurkat cells downstream of Fas-associated death domain protein (FADD) and caspase 8. Glutathione 72-75 caspase 8 Homo sapiens 164-173 17554377-8 2007 Overall, our results indicate that CD95(APO-1) induces the FADD- and caspase 8-dependent internalization of Na(+),K(+)-ATPase through intracellular GSH loss, and the subsequent generation of H(2)O(2)-mediated serine phosphorylation of Na(+),K(+)-ATPase alpha1 subunit. Glutathione 148-151 caspase 8 Homo sapiens 69-78 16040627-7 2005 Collectively, our results indicate that alpha,beta-unsaturated aldehydes can inhibit constitutive neutrophil apoptosis by common mechanisms, involving changes in cellular GSH status resulting in reduced activation of initiator caspases as well as inactivation of caspase-3 by modification of its critical cysteine residue. Glutathione 171-174 caspase 8 Homo sapiens 227-235 11021749-14 2000 These findings suggest that the As2O3 treatment activates caspase 8 in a CD95-independent but GSH concentration-dependent manner. Glutathione 94-97 caspase 8 Homo sapiens 58-67 11734564-0 2002 Glutathione dependence of caspase-8 activation at the death-inducing signaling complex. Glutathione 0-11 caspase 8 Homo sapiens 26-35 11734564-2 2002 We investigated differential effects of glutathione depletion on CD95-triggered apoptosis in T and B cell lines as well as the glutathione dependence of caspase-8 activation. Glutathione 127-138 caspase 8 Homo sapiens 153-162 11734564-9 2002 Our data indicate that the activation of caspase-8 at the DISC and hence CD95-mediated apoptosis induction shows a cell-specific requirement for intracellular glutathione. Glutathione 159-170 caspase 8 Homo sapiens 41-50 11439090-2 2001 In the highly sensitive Jurkat cell line, early caspase-8 activation, observed from 2 h after treatment, was chronologically associated with an acute depletion of glutathione and the cleavage of caspase-3 and poly-ADP ribosyl polymerase (PARP), followed by a progressive fall in the mitochondrial transmembrane potential (Delta(psi)m), between 4 and 48 h after treatment. Glutathione 163-174 caspase 8 Homo sapiens 48-57 12482880-7 2003 Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8. Glutathione 0-11 caspase 8 Homo sapiens 68-77 12482880-7 2003 Glutathione and cysteine neutralized an inhibitory effect of PCA on caspase-8, and PCA bound directly to the active center cysteine in the large subunit of caspase-8. Glutathione 0-11 caspase 8 Homo sapiens 156-165 9837855-5 1998 In addition, cell treatment with GSH impaired cytochrome c release into the cytosol and degradation of caspase-8 occurring during cell death. Glutathione 33-36 caspase 8 Homo sapiens 103-112 27551472-9 2015 Combination treatment caused a synergistic downregulation of glutathione levels and increased DNA damage, driving apoptosis via caspase 8 and 9 activation. Glutathione 61-72 caspase 8 Homo sapiens 128-137 24627148-7 2014 H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time. Glutathione 157-160 caspase 8 Homo sapiens 54-61 25915766-7 2015 Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells. Glutathione 31-34 caspase 8 Homo sapiens 113-122 24627148-7 2014 H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time. Glutathione 157-160 caspase 8 Homo sapiens 201-208 24627148-7 2014 H2O2 also increased the ROS level at 1 h, and several caspase inhibitors attenuated the increased level at 1 h but not at 6, 12 and 24 h. H2O2 decreased the GSH level in HeLa cells at 1 h, and several caspase inhibitors attenuated the decreased level of GSH at this time. Glutathione 254-257 caspase 8 Homo sapiens 54-61 24146141-9 2014 Interestingly, stimulation of GSH loss by MK571 also enhanced the initiator phase of apoptosis by stimulating initiator caspase 8 and 9 activity and pro-apoptotic BCL-2 interacting domain cleavage. Glutathione 30-33 caspase 8 Homo sapiens 120-129 23826964-6 2013 The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases. Glutathione 114-117 caspase 8 Homo sapiens 164-172