PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30703377-0	2019	Cell-specific regulation of Nrf2 during ROS-Dependent cell death caused by 2,3,5-tris(glutathion-S-yl)hydroquinone (TGHQ).	2,3,5-(triglutathion-S-yl)hydroquinone	75-114	NFE2 like bZIP transcription factor 2	Homo sapiens	28-32
3200250-10	1988	The inhibition of gamma-glutamyl transpeptidase by AT-125 protected against 2,3,5-(triglutathion-S-yl)hydroquinone-mediated nephrotoxicity.	2,3,5-(triglutathion-S-yl)hydroquinone	76-114	inactive glutathione hydrolase 2	Homo sapiens	18-47
31165168-2	2019	TGHQ generates ROS, causing DNA strand breaks, hyperactivation of PARP-1, increases in intracellular calcium ([Ca2+]i), and cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	66-72
31165168-13	2019	Nevertheless, TGHQ promoted a time-dependent translocation of TFII-I from the nucleus to the cytosol concomitant with a decrease in tyrosine phosphorylation in alpha/beta-TFII-I.	2,3,5-(triglutathion-S-yl)hydroquinone	14-18	general transcription factor IIi	Homo sapiens	62-68
31165168-13	2019	Nevertheless, TGHQ promoted a time-dependent translocation of TFII-I from the nucleus to the cytosol concomitant with a decrease in tyrosine phosphorylation in alpha/beta-TFII-I.	2,3,5-(triglutathion-S-yl)hydroquinone	14-18	general transcription factor IIi	Homo sapiens	171-177
30703377-0	2019	Cell-specific regulation of Nrf2 during ROS-Dependent cell death caused by 2,3,5-tris(glutathion-S-yl)hydroquinone (TGHQ).	2,3,5-(triglutathion-S-yl)hydroquinone	116-120	NFE2 like bZIP transcription factor 2	Homo sapiens	28-32
30703377-2	2019	We have previously detected that TGHQ induces ROS-dependent necrotic or apoptotic cell death in renal epithelial HK-2 and human leukemic HL-60 cells respectively.	2,3,5-(triglutathion-S-yl)hydroquinone	33-37	hexokinase 2	Homo sapiens	113-117
30703377-3	2019	Herein, we sought to determine the nature of the Nrf2 regulation in HK-2 and HL-60 cells undergoing TGHQ-mediated ROS-dependent cell death, due to the key role of Nrf2 in oxidative stress.	2,3,5-(triglutathion-S-yl)hydroquinone	100-104	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
30703377-3	2019	Herein, we sought to determine the nature of the Nrf2 regulation in HK-2 and HL-60 cells undergoing TGHQ-mediated ROS-dependent cell death, due to the key role of Nrf2 in oxidative stress.	2,3,5-(triglutathion-S-yl)hydroquinone	100-104	hexokinase 2	Homo sapiens	68-72
30703377-3	2019	Herein, we sought to determine the nature of the Nrf2 regulation in HK-2 and HL-60 cells undergoing TGHQ-mediated ROS-dependent cell death, due to the key role of Nrf2 in oxidative stress.	2,3,5-(triglutathion-S-yl)hydroquinone	100-104	NFE2 like bZIP transcription factor 2	Homo sapiens	163-167
26333016-7	2016	Amplification of the kinase domain of B-Raf from QTRRE cells, outer-stripe of the outer medulla of 8-month TGHQ- or vehicle-treated Tsc-2(+/+) and Tsc-2(EK/+) rats, as well as tumors excised from 8-month TGHQ-treated Tsc-2(EK/+) rats revealed three splice variants of B-Raf within the kinase domain.	2,3,5-(triglutathion-S-yl)hydroquinone	107-111	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	38-43
28525621-1	2017	2,3,5-tris(Glutathion-S-yl)hydroquinone, a potent nephrotoxic and nephrocarcinogenic metabolite of benzene and hydroquinone, generates reactive oxygen species (ROS) causing DNA strand breaks and the subsequent activation of DNA repair enzymes, including poly(ADP-ribose) polymerase (PARP)-1.	2,3,5-(triglutathion-S-yl)hydroquinone	0-39	poly(ADP-ribose) polymerase 1	Homo sapiens	254-290
26333016-7	2016	Amplification of the kinase domain of B-Raf from QTRRE cells, outer-stripe of the outer medulla of 8-month TGHQ- or vehicle-treated Tsc-2(+/+) and Tsc-2(EK/+) rats, as well as tumors excised from 8-month TGHQ-treated Tsc-2(EK/+) rats revealed three splice variants of B-Raf within the kinase domain.	2,3,5-(triglutathion-S-yl)hydroquinone	107-111	TSC complex subunit 2	Rattus norvegicus	132-137
22523229-2	2012	We now report that TGHQ induces severe DNA damage, as evidenced by DNA ladder formation and H2AX phosphorylation.	2,3,5-(triglutathion-S-yl)hydroquinone	19-23	H2A.X variant histone	Homo sapiens	92-96
24752504-3	2014	We have utilized a model in which 2,3,5-tris(glutathion-S-yl)hydroquinone (TGHQ), a nephrotoxic and nephrocarcinogenic metabolite of hydroquinone, causes ROS-dependent cell death in human renal proximal tubule epithelial cells (HK-2), to further elucidate the role of PARP-1 in ROS-dependent cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	34-73	poly(ADP-ribose) polymerase 1	Homo sapiens	268-274
24752504-3	2014	We have utilized a model in which 2,3,5-tris(glutathion-S-yl)hydroquinone (TGHQ), a nephrotoxic and nephrocarcinogenic metabolite of hydroquinone, causes ROS-dependent cell death in human renal proximal tubule epithelial cells (HK-2), to further elucidate the role of PARP-1 in ROS-dependent cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	75-79	poly(ADP-ribose) polymerase 1	Homo sapiens	268-274
24752504-5	2014	Thus, inhibition of PARP-1 with PJ34 completely blocked TGHQ-mediated accumulation of poly(ADP-ribose) polymers and NAD consumption, and delayed HK-2 cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	56-60	poly(ADP-ribose) polymerase 1	Homo sapiens	20-26
24752504-8	2014	Conversely, inhibition of PARP-1 modulated TGHQ-mediated changes in Ca(2+) homeostasis.	2,3,5-(triglutathion-S-yl)hydroquinone	43-47	poly(ADP-ribose) polymerase 1	Homo sapiens	26-32
22523229-4	2012	PJ-34 (a PARP-1 inhibitor) completely prevented the formation of PARs, partially attenuated TGHQ-mediated ATP depletion, but had little effect on NAD depletion.	2,3,5-(triglutathion-S-yl)hydroquinone	92-96	poly(ADP-ribose) polymerase 1	Homo sapiens	9-15
22523229-6	2012	Indeed, PARP-1 inhibition reduced TGHQ-induced caspase-3, -7, and -9 activation, at least partially by attenuating cytochrome c translocation from mitochondria to the cytoplasm.	2,3,5-(triglutathion-S-yl)hydroquinone	34-38	poly(ADP-ribose) polymerase 1	Homo sapiens	8-14
22523229-6	2012	Indeed, PARP-1 inhibition reduced TGHQ-induced caspase-3, -7, and -9 activation, at least partially by attenuating cytochrome c translocation from mitochondria to the cytoplasm.	2,3,5-(triglutathion-S-yl)hydroquinone	34-38	caspase 3	Homo sapiens	47-68
22523229-6	2012	Indeed, PARP-1 inhibition reduced TGHQ-induced caspase-3, -7, and -9 activation, at least partially by attenuating cytochrome c translocation from mitochondria to the cytoplasm.	2,3,5-(triglutathion-S-yl)hydroquinone	34-38	cytochrome c, somatic	Homo sapiens	115-127
22523229-7	2012	In contrast, PJ-34 potentiated TGHQ-induced caspase-8 activation, suggesting that PARP-1 plays a dual role in regulating TGHQ-induced apoptosis via opposing effects on the intrinsic (mitochondrial) and extrinsic (death-receptor) pathways.	2,3,5-(triglutathion-S-yl)hydroquinone	31-35	caspase 8	Homo sapiens	44-53
22523229-7	2012	In contrast, PJ-34 potentiated TGHQ-induced caspase-8 activation, suggesting that PARP-1 plays a dual role in regulating TGHQ-induced apoptosis via opposing effects on the intrinsic (mitochondrial) and extrinsic (death-receptor) pathways.	2,3,5-(triglutathion-S-yl)hydroquinone	31-35	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
22523229-7	2012	In contrast, PJ-34 potentiated TGHQ-induced caspase-8 activation, suggesting that PARP-1 plays a dual role in regulating TGHQ-induced apoptosis via opposing effects on the intrinsic (mitochondrial) and extrinsic (death-receptor) pathways.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
22523229-10	2012	In summary, TGHQ-induced apoptosis of HL-60 cells is accompanied by PARP-1, caspase activation, and AIF nuclear translocation.	2,3,5-(triglutathion-S-yl)hydroquinone	12-16	poly(ADP-ribose) polymerase 1	Homo sapiens	68-74
22523229-11	2012	TGHQ-induced apoptosis appears to primarily occur via engagement of the mitochondrial-mediated pathway in a process amenable to PARP inhibition.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	poly(ADP-ribose) polymerase 1	Homo sapiens	128-132
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	cyclin D1	Rattus norvegicus	151-160
21813464-3	2011	Critical proteins in both pathways are activated following treatment of Eker rats (Tsc-2(EK/+)) with the nephrocarcinogen 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ), which also results in loss of the wild-type allele of Tsc-2 in renal preneoplastic lesions and tumors.	2,3,5-(triglutathion-S-yl)hydroquinone	122-162	TSC complex subunit 2	Rattus norvegicus	83-88
21813464-3	2011	Critical proteins in both pathways are activated following treatment of Eker rats (Tsc-2(EK/+)) with the nephrocarcinogen 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ), which also results in loss of the wild-type allele of Tsc-2 in renal preneoplastic lesions and tumors.	2,3,5-(triglutathion-S-yl)hydroquinone	122-162	TSC complex subunit 2	Rattus norvegicus	225-230
21813464-3	2011	Critical proteins in both pathways are activated following treatment of Eker rats (Tsc-2(EK/+)) with the nephrocarcinogen 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ), which also results in loss of the wild-type allele of Tsc-2 in renal preneoplastic lesions and tumors.	2,3,5-(triglutathion-S-yl)hydroquinone	164-168	TSC complex subunit 2	Rattus norvegicus	83-88
21813464-3	2011	Critical proteins in both pathways are activated following treatment of Eker rats (Tsc-2(EK/+)) with the nephrocarcinogen 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ), which also results in loss of the wild-type allele of Tsc-2 in renal preneoplastic lesions and tumors.	2,3,5-(triglutathion-S-yl)hydroquinone	164-168	TSC complex subunit 2	Rattus norvegicus	225-230
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	TSC complex subunit 2	Rattus norvegicus	69-74
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	B-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	131-136
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	138-143
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	162-167
21813464-4	2011	Western blot analysis of kidney tumors formed following treatment of Tsc-2(EK/+) rats with TGHQ for 8 months revealed increases in B-Raf, Raf-1, pERK, cyclin D1, 4EBP1, and p-4EBP1-Ser65, -Thr70, and -Thr37/46 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	91-95	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	175-180
21813464-5	2011	Similar changes are observed following TGHQ-mediated transformation of primary renal epithelial cells derived from Tsc-2(EK/+) rats (quinol-thioether rat renal epithelial [QTRRE] cells) that are also null for tuberin.	2,3,5-(triglutathion-S-yl)hydroquinone	39-43	TSC complex subunit 2	Rattus norvegicus	115-120
15800030-0	2005	2,3,5-tris(Glutathion-S-yl)hydroquinone (TGHQ)-mediated apoptosis of human promyelocytic leukemia cells is preceded by mitochondrial cytochrome c release in the absence of a decrease in the mitochondrial membrane potential.	2,3,5-(triglutathion-S-yl)hydroquinone	41-45	cytochrome c, somatic	Homo sapiens	133-145
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	26-66	TSC complex subunit 2	Rattus norvegicus	82-87
21135414-3	2011	To assist in elucidating the contribution of reactive oxygen species (ROS) to TGHQ-induced toxicity, we determined whether the antioxidant, N-acetyl-L-cysteine (NAC), could protect human kidney proximal tubule epithelial cells (HK-2 cell line) against TGHQ-induced toxicity.	2,3,5-(triglutathion-S-yl)hydroquinone	252-256	X-linked Kx blood group	Homo sapiens	161-164
21135414-4	2011	NAC provided remarkable protection against TGHQ-induced toxicity to HK-2 cells.	2,3,5-(triglutathion-S-yl)hydroquinone	43-47	X-linked Kx blood group	Homo sapiens	0-3
21135414-5	2011	NAC almost completely inhibited TGHQ-induced cell death, mitochondrial membrane potential collapse, as well as ROS production.	2,3,5-(triglutathion-S-yl)hydroquinone	32-36	X-linked Kx blood group	Homo sapiens	0-3
21135414-6	2011	NAC also attenuated TGHQ-induced DNA damage and the subsequent activation of poly (ADP-ribose) polymerase and ATP depletion.	2,3,5-(triglutathion-S-yl)hydroquinone	20-24	X-linked Kx blood group	Homo sapiens	0-3
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	26-66	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	161-164
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	26-66	cyclin D1	Rattus norvegicus	203-212
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	68-72	TSC complex subunit 2	Rattus norvegicus	82-87
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	68-72	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	161-164
21693435-3	2011	Renal tumors derived from 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-treated Tsc-2(EK/+) rats, and null for tuberin, display elevated nuclear and cytosolic p27, with parallel increases in cytosolic cyclin D1 levels.	2,3,5-(triglutathion-S-yl)hydroquinone	68-72	cyclin D1	Rattus norvegicus	203-212
15800030-0	2005	2,3,5-tris(Glutathion-S-yl)hydroquinone (TGHQ)-mediated apoptosis of human promyelocytic leukemia cells is preceded by mitochondrial cytochrome c release in the absence of a decrease in the mitochondrial membrane potential.	2,3,5-(triglutathion-S-yl)hydroquinone	0-39	cytochrome c, somatic	Homo sapiens	133-145
15800030-4	2005	Western blot analysis revealed the complete disappearance of pro-caspase 9 between 1 and 2 hours after exposure of HL-60 cells to TGHQ, concomitant with the appearance of cleaved caspase 9 and increases in caspase 9 activity.	2,3,5-(triglutathion-S-yl)hydroquinone	130-134	caspase 9	Homo sapiens	65-74
15800030-4	2005	Western blot analysis revealed the complete disappearance of pro-caspase 9 between 1 and 2 hours after exposure of HL-60 cells to TGHQ, concomitant with the appearance of cleaved caspase 9 and increases in caspase 9 activity.	2,3,5-(triglutathion-S-yl)hydroquinone	130-134	caspase 9	Homo sapiens	179-188
15800030-4	2005	Western blot analysis revealed the complete disappearance of pro-caspase 9 between 1 and 2 hours after exposure of HL-60 cells to TGHQ, concomitant with the appearance of cleaved caspase 9 and increases in caspase 9 activity.	2,3,5-(triglutathion-S-yl)hydroquinone	130-134	caspase 9	Homo sapiens	179-188
15800030-6	2005	Levels of the anti-apoptotic Bcl-2 protein remained constant during TGHQ-induced apoptosis of HL-60 cells, but Bcl-2 S70 phosphorylation decreased.	2,3,5-(triglutathion-S-yl)hydroquinone	68-72	BCL2 apoptosis regulator	Homo sapiens	29-34
15226155-3	2004	Because TGHQ, but not epidermal growth factor (EGF), induces histone H3 phosphorylation and cell death in LLC-PK(1) cells, we hypothesized that there are differences in the mechanisms by which TGHQ and EGF induce activation of the EGF receptor (EGFR).	2,3,5-(triglutathion-S-yl)hydroquinone	8-12	epidermal growth factor	Homo sapiens	202-205
15226156-8	2004	Moreover, TGHQ-induced p38 MAPK activation is disrupted under conditions of a compromised ER stress response in pkASgrp78 cells, which likely contributes to the loss of cytoprotection.	2,3,5-(triglutathion-S-yl)hydroquinone	10-14	mitogen-activated protein kinase 14	Homo sapiens	23-26
15226155-3	2004	Because TGHQ, but not epidermal growth factor (EGF), induces histone H3 phosphorylation and cell death in LLC-PK(1) cells, we hypothesized that there are differences in the mechanisms by which TGHQ and EGF induce activation of the EGF receptor (EGFR).	2,3,5-(triglutathion-S-yl)hydroquinone	8-12	epidermal growth factor receptor	Homo sapiens	231-243
15226155-3	2004	Because TGHQ, but not epidermal growth factor (EGF), induces histone H3 phosphorylation and cell death in LLC-PK(1) cells, we hypothesized that there are differences in the mechanisms by which TGHQ and EGF induce activation of the EGF receptor (EGFR).	2,3,5-(triglutathion-S-yl)hydroquinone	8-12	epidermal growth factor receptor	Homo sapiens	245-249
15226155-8	2004	In untransfected, pcDNA3 or pcDNA3-p38 (native)-transfected LLC-PK(1) cells, Hsp27 was intensively phosphorylated after TGHQ treatment, whereas in pcDNA3-DNp38-transfected cells, TGHQ failed to induce Hsp27 phosphorylation.	2,3,5-(triglutathion-S-yl)hydroquinone	120-124	mitogen-activated protein kinase 1	Homo sapiens	35-38
15226155-8	2004	In untransfected, pcDNA3 or pcDNA3-p38 (native)-transfected LLC-PK(1) cells, Hsp27 was intensively phosphorylated after TGHQ treatment, whereas in pcDNA3-DNp38-transfected cells, TGHQ failed to induce Hsp27 phosphorylation.	2,3,5-(triglutathion-S-yl)hydroquinone	120-124	heat shock protein family B (small) member 1	Homo sapiens	77-82
15226155-8	2004	In untransfected, pcDNA3 or pcDNA3-p38 (native)-transfected LLC-PK(1) cells, Hsp27 was intensively phosphorylated after TGHQ treatment, whereas in pcDNA3-DNp38-transfected cells, TGHQ failed to induce Hsp27 phosphorylation.	2,3,5-(triglutathion-S-yl)hydroquinone	179-183	heat shock protein family B (small) member 1	Homo sapiens	77-82
15226155-9	2004	Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.	2,3,5-(triglutathion-S-yl)hydroquinone	71-75	epidermal growth factor receptor	Homo sapiens	5-9
15226155-9	2004	Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.	2,3,5-(triglutathion-S-yl)hydroquinone	71-75	mitogen-activated protein kinase 1	Homo sapiens	22-25
15226155-9	2004	Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.	2,3,5-(triglutathion-S-yl)hydroquinone	71-75	epidermal growth factor receptor	Homo sapiens	35-39
15226155-9	2004	Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.	2,3,5-(triglutathion-S-yl)hydroquinone	71-75	mitogen-activated protein kinase 3	Homo sapiens	50-56
15226155-9	2004	Thus EGFR-independent p38 MAPK and EGFR-dependent ERK1/2 activation by TGHQ lead to the activation of two downstream signaling factors, i.e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin.	2,3,5-(triglutathion-S-yl)hydroquinone	71-75	heat shock protein family B (small) member 1	Homo sapiens	157-162
12663520-10	2003	Interestingly, whereas OGG1 expression was rapidly (4 h) induced in Tsc-2(+/+) rats following exposure to TGHQ, it was significantly reduced in Tsc-2(EK/+) rats.	2,3,5-(triglutathion-S-yl)hydroquinone	106-110	8-oxoguanine DNA glycosylase	Rattus norvegicus	23-27
15129024-0	2004	Induction of ERK1/2 and histone H3 phosphorylation within the outer stripe of the outer medulla of the Eker rat by 2,3,5-tris-(glutathion-S-yl)hydroquinone.	2,3,5-(triglutathion-S-yl)hydroquinone	115-155	mitogen activated protein kinase 3	Rattus norvegicus	13-19
15129024-4	2004	Using the Eker (Tsc-2 mutant) rat as a model, we show by immunohistochemistry that TGHQ (7.5 micromol/kg) selectively induces ERK1/2 phosphorylation within the outer stripe of the outer medulla (OSOM) of the kidney.	2,3,5-(triglutathion-S-yl)hydroquinone	83-87	TSC complex subunit 2	Rattus norvegicus	16-21
15129024-4	2004	Using the Eker (Tsc-2 mutant) rat as a model, we show by immunohistochemistry that TGHQ (7.5 micromol/kg) selectively induces ERK1/2 phosphorylation within the outer stripe of the outer medulla (OSOM) of the kidney.	2,3,5-(triglutathion-S-yl)hydroquinone	83-87	mitogen activated protein kinase 3	Rattus norvegicus	126-132
12663520-10	2003	Interestingly, whereas OGG1 expression was rapidly (4 h) induced in Tsc-2(+/+) rats following exposure to TGHQ, it was significantly reduced in Tsc-2(EK/+) rats.	2,3,5-(triglutathion-S-yl)hydroquinone	106-110	TSC complex subunit 2	Rattus norvegicus	68-73
12663520-11	2003	The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	8-oxoguanine DNA glycosylase	Rattus norvegicus	172-176
12663520-11	2003	The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	TSC complex subunit 2	Rattus norvegicus	191-196
12663520-11	2003	The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	TSC complex subunit 2	Rattus norvegicus	191-196
12663520-11	2003	The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	8-oxoguanine DNA glycosylase	Rattus norvegicus	172-176
12663520-11	2003	The combination of the higher constitutive expression of OGG1 in Tsc-2(+/+) rats, and its rapid induction in response to TGHQ treatment, coupled to the initial decrease in OGG1 expression in Tsc-2(EK/+) rats, results in Tsc-2(EK/+) OGG1 protein levels just 5% of those seen in Tsc-2(+/+) rats 8 h after treatment.	2,3,5-(triglutathion-S-yl)hydroquinone	121-125	TSC complex subunit 2	Rattus norvegicus	191-196
12663520-12	2003	Coincidentally, 8-oxo-dG levels in Tsc-2(+/+) rats 8 h after treatment with TGHQ are just 5% of those that occur in Tsc-2(EK/+) rats.	2,3,5-(triglutathion-S-yl)hydroquinone	76-80	TSC complex subunit 2	Rattus norvegicus	35-40
12663520-14	2003	In keeping with this view, acute TGHQ-induced cytotoxicity was greater in Tsc-2(EK/+) rats than in Tsc-2(+/+) rats.	2,3,5-(triglutathion-S-yl)hydroquinone	33-37	TSC complex subunit 2	Rattus norvegicus	74-79
12663520-14	2003	In keeping with this view, acute TGHQ-induced cytotoxicity was greater in Tsc-2(EK/+) rats than in Tsc-2(+/+) rats.	2,3,5-(triglutathion-S-yl)hydroquinone	33-37	TSC complex subunit 2	Rattus norvegicus	99-104
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	194-234	mitogen-activated protein kinase 14	Homo sapiens	90-126
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	194-234	mitogen-activated protein kinase 3	Homo sapiens	128-132
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	194-234	mitogen-activated protein kinase 3	Homo sapiens	40-46
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	194-234	mitogen-activated protein kinase 8	Homo sapiens	75-83
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	236-240	mitogen-activated protein kinase 14	Homo sapiens	90-126
12482247-1	2002	Extracellular signal-regulated kinases (ERK1/2), c-Jun N-terminal kinases (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK) were all rapidly activated in a ROS-dependent manner during 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ)-mediated oxidative stress and oncotic cell death in renal proximal tubule epithelial cells (LLC-PK1).	2,3,5-(triglutathion-S-yl)hydroquinone	236-240	mitogen-activated protein kinase 3	Homo sapiens	128-132
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	mitogen-activated protein kinase 3	Homo sapiens	32-38
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	mitogen-activated protein kinase 8	Homo sapiens	43-46
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	epidermal growth factor receptor	Homo sapiens	62-94
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	epidermal growth factor receptor	Homo sapiens	96-100
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	mitogen-activated protein kinase 1	Homo sapiens	122-125
12482247-2	2002	TGHQ-induced phosphorylation of ERK1/2 and JNK MAPKs required epidermal growth factor receptor (EGFR) activation, whereas p38 MAPK activation was EGFR independent.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	epidermal growth factor receptor	Homo sapiens	146-150
12482247-3	2002	In contrast to their established roles in cell survival, TGHQ-activated ERK1/2 and p38 MAPK (but not JNK) appear to contribute to cell death, since inhibition of ERK1/2 or p38 MAPKs with PD098059 or SB202190 respectively, attenuated TGHQ-mediated cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	57-61	mitogen-activated protein kinase 3	Homo sapiens	72-78
12482247-3	2002	In contrast to their established roles in cell survival, TGHQ-activated ERK1/2 and p38 MAPK (but not JNK) appear to contribute to cell death, since inhibition of ERK1/2 or p38 MAPKs with PD098059 or SB202190 respectively, attenuated TGHQ-mediated cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	57-61	mitogen-activated protein kinase 1	Homo sapiens	83-86
12482247-3	2002	In contrast to their established roles in cell survival, TGHQ-activated ERK1/2 and p38 MAPK (but not JNK) appear to contribute to cell death, since inhibition of ERK1/2 or p38 MAPKs with PD098059 or SB202190 respectively, attenuated TGHQ-mediated cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	57-61	mitogen-activated protein kinase 3	Homo sapiens	162-168
12482247-3	2002	In contrast to their established roles in cell survival, TGHQ-activated ERK1/2 and p38 MAPK (but not JNK) appear to contribute to cell death, since inhibition of ERK1/2 or p38 MAPKs with PD098059 or SB202190 respectively, attenuated TGHQ-mediated cell death.	2,3,5-(triglutathion-S-yl)hydroquinone	57-61	mitogen-activated protein kinase 1	Homo sapiens	172-175
12482247-4	2002	TGHQ increased AP-1 and NFkappaB DNA-binding activity, but whereas pharmacological inhibition of ERK1/2 or p38 MAPKs attenuated AP-1 DNA binding activity, it potentiated TGHQ-mediated NFkappaB activation.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-19
12482247-4	2002	TGHQ increased AP-1 and NFkappaB DNA-binding activity, but whereas pharmacological inhibition of ERK1/2 or p38 MAPKs attenuated AP-1 DNA binding activity, it potentiated TGHQ-mediated NFkappaB activation.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	nuclear factor kappa B subunit 1	Homo sapiens	24-32
11453727-9	2001	In contrast, pretreatment of cells with (PD098059), a mitogen activated protein kinase kinase (MEK) inhibitor, markedly reduced TGHQ-mediated TRE-binding activity, but enhanced TGHQ-mediated NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	128-132	mitogen-activated protein kinase kinase 7	Homo sapiens	54-93
11453727-2	2001	Studies were conducted to determine whether the oxidative stress induced by TGHQ in renal proximal tubule epithelial cells (LLC-PK(1)) modulates transcriptional activities widely implicated in transformation responses, namely 12-O-tetradecanoyl phorbol 13-acetate (TPA) responsive element (TRE)- and nuclear factor kappa B (NF-kappaB)-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	76-80	nuclear factor kappa B subunit 1	Homo sapiens	324-333
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	9-49	TSC complex subunit 2	Rattus norvegicus	200-204
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	9-49	TSC complex subunit 2	Rattus norvegicus	233-237
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	9-49	TSC complex subunit 2	Rattus norvegicus	233-237
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	51-55	TSC complex subunit 2	Rattus norvegicus	200-204
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	51-55	TSC complex subunit 2	Rattus norvegicus	233-237
12110509-1	2002	Although 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ; 2.5 micromol/kg ip) markedly increased cell proliferation within the outer stripe of the outer medulla (OSOM) of the kidney in both wild-type (Tsc2(+/+)) and mutant Eker rats (Tsc2(EK/+)), only TGHQ-treated Tsc2(EK/+) rats developed renal tumors, indicating that cell proliferation per se was not sufficient for tumor development.	2,3,5-(triglutathion-S-yl)hydroquinone	51-55	TSC complex subunit 2	Rattus norvegicus	233-237
12110509-4	2002	Cyclin D1 was also highly expressed in TGHQ-induced renal tumors.	2,3,5-(triglutathion-S-yl)hydroquinone	39-43	cyclin D1	Rattus norvegicus	0-9
11453727-4	2001	Catalase fully inhibited peak TGHQ-mediated TRE- and NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	30-34	catalase	Homo sapiens	0-8
11453727-4	2001	Catalase fully inhibited peak TGHQ-mediated TRE- and NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	30-34	nuclear factor kappa B subunit 1	Homo sapiens	53-62
11453727-9	2001	In contrast, pretreatment of cells with (PD098059), a mitogen activated protein kinase kinase (MEK) inhibitor, markedly reduced TGHQ-mediated TRE-binding activity, but enhanced TGHQ-mediated NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	128-132	mitogen-activated protein kinase kinase 7	Homo sapiens	95-98
11453727-9	2001	In contrast, pretreatment of cells with (PD098059), a mitogen activated protein kinase kinase (MEK) inhibitor, markedly reduced TGHQ-mediated TRE-binding activity, but enhanced TGHQ-mediated NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	177-181	mitogen-activated protein kinase kinase 7	Homo sapiens	54-93
11453727-9	2001	In contrast, pretreatment of cells with (PD098059), a mitogen activated protein kinase kinase (MEK) inhibitor, markedly reduced TGHQ-mediated TRE-binding activity, but enhanced TGHQ-mediated NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	177-181	mitogen-activated protein kinase kinase 7	Homo sapiens	95-98
11453727-9	2001	In contrast, pretreatment of cells with (PD098059), a mitogen activated protein kinase kinase (MEK) inhibitor, markedly reduced TGHQ-mediated TRE-binding activity, but enhanced TGHQ-mediated NF-kappaB-binding activity.	2,3,5-(triglutathion-S-yl)hydroquinone	177-181	nuclear factor kappa B subunit 1	Homo sapiens	191-200
10688535-9	2000	Consistent with the ability of TGHQ to generate an oxidative stress, both deferoxamine mesylate and catalase protect LLC-PK(1) cells from TGHQ-mediated cytotoxicity.	2,3,5-(triglutathion-S-yl)hydroquinone	138-142	catalase	Homo sapiens	100-108
11170505-11	2001	Loss of heterozygosity (LOH) at the Tsc-2 locus was demonstrated in both the toxic tubular dysplasias and tumors from rats treated with TGHQ for 10 months, consistent with TGHQ-induced loss of tumor suppressor function of the Tsc-2 gene.	2,3,5-(triglutathion-S-yl)hydroquinone	136-140	TSC complex subunit 2	Rattus norvegicus	36-41
11170505-11	2001	Loss of heterozygosity (LOH) at the Tsc-2 locus was demonstrated in both the toxic tubular dysplasias and tumors from rats treated with TGHQ for 10 months, consistent with TGHQ-induced loss of tumor suppressor function of the Tsc-2 gene.	2,3,5-(triglutathion-S-yl)hydroquinone	136-140	TSC complex subunit 2	Rattus norvegicus	226-231
11170505-11	2001	Loss of heterozygosity (LOH) at the Tsc-2 locus was demonstrated in both the toxic tubular dysplasias and tumors from rats treated with TGHQ for 10 months, consistent with TGHQ-induced loss of tumor suppressor function of the Tsc-2 gene.	2,3,5-(triglutathion-S-yl)hydroquinone	172-176	TSC complex subunit 2	Rattus norvegicus	36-41
11170505-11	2001	Loss of heterozygosity (LOH) at the Tsc-2 locus was demonstrated in both the toxic tubular dysplasias and tumors from rats treated with TGHQ for 10 months, consistent with TGHQ-induced loss of tumor suppressor function of the Tsc-2 gene.	2,3,5-(triglutathion-S-yl)hydroquinone	172-176	TSC complex subunit 2	Rattus norvegicus	226-231
10688535-10	2000	Only catalase, however, completely blocks TGHQ-mediated PGE(2) synthesis, implying a major role for hydrogen peroxide in this response.	2,3,5-(triglutathion-S-yl)hydroquinone	42-46	catalase	Homo sapiens	5-13
10688535-11	2000	TGHQ induces the early (60 min) expression of gadd153 and hsp70.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	DNA damage inducible transcript 3	Homo sapiens	46-53
10688535-11	2000	TGHQ induces the early (60 min) expression of gadd153 and hsp70.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	heat shock protein family A (Hsp70) member 4	Homo sapiens	58-63
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	124-128	DNA damage inducible transcript 3	Homo sapiens	184-191
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	124-128	heat shock protein family A (Hsp70) member 4	Homo sapiens	196-201
10688535-14	2000	In addition, catalase and, to a lesser extent, deferoxamine mesylate block TGHQ-induced gene expression.	2,3,5-(triglutathion-S-yl)hydroquinone	75-79	catalase	Homo sapiens	13-21
9450487-11	1997	Consistent with this view, 2,3,5-(tris-glutathion-S-yl)hydroquinone, a metabolite of hydroquinone, causes increases in BUN, urinary gamma-GT and ALP, all of which are maximal 12 h after administration of 2,3,5-(tris-glutathion-S-yl)hydroquinone.	2,3,5-(triglutathion-S-yl)hydroquinone	27-67	gamma-glutamyltransferase 1	Rattus norvegicus	132-140