PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17618106-8	2008	Taken together, these data demonstrate a novel correlation between GSH levels and Akt activation in T lymphocyte survival, which involves FasL down-regulation and c-FLIP(S) expression through increasing intracellular GSH levels.	Glutathione	67-70	Fas ligand	Homo sapiens	138-142	
18940791-5	2008	GSH depletion in response to FasL was paralleled by distinct degrees of AVD identified by differences in cellular forward scatter and electronic impedance analysis.	Glutathione	0-3	Fas ligand	Homo sapiens	29-33	
29565452-8	2018	Furthermore, pretreatment of Caki cells with ROS scavengers (N-acetylcysteine and glutathione) prevented the downregulation of cFLIP(L), the upregulation of cFLIP(S) and apoptosis induced by FasL.	Glutathione	82-93	Fas ligand	Homo sapiens	191-195	
18497573-10	2008	After adding FasL/Act D, increased caspases activities, lipid preoxidation and reduced GSH level, as well as mitochondrial release of cytochrome c were found in Ad-CYP2E1 infected cells (all p < 0.01); these changes were significantly attenuated by DAS (all p < 0.05).	Glutathione	87-90	Fas ligand	Homo sapiens	13-17	
10497012-8	1999	Furthermore, because VK(3) effects were inhibited by glutathione, a potent antioxidant, oxidative stress was linked to the Fas/FasL system.	Glutathione	53-64	Fas ligand	Homo sapiens	127-131	
17554377-6	2007	GSH depletion in Fas L-treated Jurkat cells induced the generation of hydrogen peroxide (H(2)O(2)), which subsequently increased the serine phosphorylation of Na(+),K(+)-ATPase alpha1 subunit.	Glutathione	0-3	Fas ligand	Homo sapiens	17-22	
10711676-11	2000	Glutathione and NAC completely abrogated tBH-induced increase in FasL and Fas expression and apoptosis.	Glutathione	0-11	Fas ligand	Homo sapiens	65-69	
16857677-0	2006	SLCO/OATP-like transport of glutathione in FasL-induced apoptosis: glutathione efflux is coupled to an organic anion exchange and is necessary for the progression of the execution phase of apoptosis.	Glutathione	28-39	Fas ligand	Homo sapiens	43-47	
16857677-0	2006	SLCO/OATP-like transport of glutathione in FasL-induced apoptosis: glutathione efflux is coupled to an organic anion exchange and is necessary for the progression of the execution phase of apoptosis.	Glutathione	67-78	Fas ligand	Homo sapiens	43-47	
16857677-3	2006	We have studied this issue using Fas ligand (FasL)-induced apoptosis in Jurkat cells where changes in [GSH](i) can be analyzed biochemically and at the single cell level by flow cytometry.	Glutathione	103-106	Fas ligand	Homo sapiens	33-43	
16857677-3	2006	We have studied this issue using Fas ligand (FasL)-induced apoptosis in Jurkat cells where changes in [GSH](i) can be analyzed biochemically and at the single cell level by flow cytometry.	Glutathione	103-106	Fas ligand	Homo sapiens	45-49	
16857677-4	2006	A reduction in the total [GSH](i) in response to FasL occurs in two distinct stages prior to the loss of membrane integrity.	Glutathione	26-29	Fas ligand	Homo sapiens	49-53	
16857677-6	2006	Glutathione loss and its accumulation in the extracellular medium, induced by FasL, was trans-stimulated by the organic substrates MK571, probenecid, taurocholic acid, estrone sulfate, and bromosulfophthalein and inhibited by high concentrations of extracellular GSH.	Glutathione	0-11	Fas ligand	Homo sapiens	78-82	
16857677-6	2006	Glutathione loss and its accumulation in the extracellular medium, induced by FasL, was trans-stimulated by the organic substrates MK571, probenecid, taurocholic acid, estrone sulfate, and bromosulfophthalein and inhibited by high concentrations of extracellular GSH.	Glutathione	263-266	Fas ligand	Homo sapiens	78-82	
16857677-7	2006	Single cell analysis demonstrated that intracellular GSH loss was paralleled by the activation of an organic anion uptake process, supporting the role of an anion exchange mechanism (SLCO/OATP-like transport) in GSH efflux induced by FasL.	Glutathione	53-56	Fas ligand	Homo sapiens	234-238	
16857677-7	2006	Single cell analysis demonstrated that intracellular GSH loss was paralleled by the activation of an organic anion uptake process, supporting the role of an anion exchange mechanism (SLCO/OATP-like transport) in GSH efflux induced by FasL.	Glutathione	212-215	Fas ligand	Homo sapiens	234-238	
16857677-10	2006	Together these results suggest that GSH efflux during FasL-induced apoptosis is mediated by a SLCO/OATP-like transport mechanism that modulates the progression of the execution phase of apoptosis.	Glutathione	36-39	Fas ligand	Homo sapiens	54-58	
10381639-3	1999	Preincubation of chemosensitive cells with antioxidants such as N-acetyl-cysteine (NAC) or glutathione (GSH), significantly reduced doxorubicin-induced apoptosis, hyperexpression of ROS, loss of mitochondrial membrane potential (DeltaPsim) and upregulation of CD95-L expression.	Glutathione	91-102	Fas ligand	Homo sapiens	260-266	
10381639-3	1999	Preincubation of chemosensitive cells with antioxidants such as N-acetyl-cysteine (NAC) or glutathione (GSH), significantly reduced doxorubicin-induced apoptosis, hyperexpression of ROS, loss of mitochondrial membrane potential (DeltaPsim) and upregulation of CD95-L expression.	Glutathione	104-107	Fas ligand	Homo sapiens	260-266	
10381639-5	1999	Downregulation of intracellular GSH concentrations reversed deficient drug-induced hyperproduction of ROS and CD95-L upregulation.	Glutathione	32-35	Fas ligand	Homo sapiens	110-116	
9247148-3	1997	Cyclosporin A interfered with CD95L expression, Ascorbic Acid and Glutathione inhibited cell death triggered by CD95/CD95L interaction; Genistein and PNU152518 acted on both steps.	Glutathione	66-77	Fas ligand	Homo sapiens	117-122	
8805638-4	1996	The thiol antioxidants N-acetyl cysteine and glutathione blocked Fas-induced death triggered via cross-linking either by IgM anti-Fas or cell-bound FasL, while the other inhibitors of activation-induced death did not block this late lethal step.	Glutathione	45-56	Fas ligand	Homo sapiens	148-152