PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30285714-6	2018	Moreover, TCE inhibited the H2O2-induced mitogen-activated protein kinase signaling pathway, resulting in the inhibition of c-Jun, c-Fos, matrix metalloproteinase (MMP)-1, MMP-3, MMP-9, and cyclooxygenase-2 expression.	Hydrogen Peroxide	28-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-129	
31387985-0	2019	Hydrogen peroxide inducible clone-5 sustains NADPH oxidase-dependent reactive oxygen species-c-jun N-terminal kinase signaling in hepatocellular carcinoma.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	93-98	
31181780-6	2019	LE treatment also significantly prevented alterations in transepithelial electrical resistance values and mRNA levels of glutathione-S-transferase (GST), c-Jun, and NFkappaB after treatment with H2O2 in ALI-cultured Calu-3 cells.	Hydrogen Peroxide	195-199	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159	
30515697-0	2019	Effects of JUN and NFE2L2 knockdown on oxidative status and NFE2L2/AP-1 targets expression in HeLa cells in basal conditions and upon sub-lethal hydrogen peroxide treatment.	Hydrogen Peroxide	145-162	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-71	
24750999-8	2014	Niclosamide pretreatment also induced c-Jun and its phosphorylation in the presence of H2O2, thereby enhancing apoptosis.	Hydrogen Peroxide	87-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	38-43	
26784015-7	2016	By using gene silencing/overexpression and scavenging/inhibitory agents, we demonstrated that MS5 induced hydrogen peroxide-mediated c-Jun-dependent Glo1 up-regulation which resulted in a decrease in the Argpyrimidine-modified Hsp70 protein level which triggered EMT in a novel mechanism involving miR-21 and SMAD signalling.	Hydrogen Peroxide	106-123	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-138	
26439801-3	2015	Here we show that hyperglycemia increases the hydrogen peroxide (H2O2) concentration through up-regulation of manganese superoxide dismutase (SOD2) expression, which further activates the ERK and p38 MAPK pathways, as well as the transcription factors NF-kappaB and AP-1, in a time-dependent manner.	Hydrogen Peroxide	46-63	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	266-270	
26439801-3	2015	Here we show that hyperglycemia increases the hydrogen peroxide (H2O2) concentration through up-regulation of manganese superoxide dismutase (SOD2) expression, which further activates the ERK and p38 MAPK pathways, as well as the transcription factors NF-kappaB and AP-1, in a time-dependent manner.	Hydrogen Peroxide	65-69	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	266-270	
29909290-5	2018	Interestingly, we found that H2O2-mediated REDD1 induction was transcriptionally regulated by activator protein-1 (AP-1), and that overexpression of c-Jun increased REDD1 protein levels and REDD1 promoter-driven luciferase activity.	Hydrogen Peroxide	29-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-113	
29909290-5	2018	Interestingly, we found that H2O2-mediated REDD1 induction was transcriptionally regulated by activator protein-1 (AP-1), and that overexpression of c-Jun increased REDD1 protein levels and REDD1 promoter-driven luciferase activity.	Hydrogen Peroxide	29-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	115-119	
29909290-5	2018	Interestingly, we found that H2O2-mediated REDD1 induction was transcriptionally regulated by activator protein-1 (AP-1), and that overexpression of c-Jun increased REDD1 protein levels and REDD1 promoter-driven luciferase activity.	Hydrogen Peroxide	29-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	149-154	
27208880-4	2016	Activation of NF-kappaB and AP-1, demonstrated by electrophoretic mobility shift assay, abolition of AT1R expression by their inhibitors, Bay-11-7085 and SR11302, respectively, and luciferase and chromatin immunoprecipitation assays confirmed transcriptional control of AT1R by NF-kappaB and AP-1 in H2O2-treated cells.	Hydrogen Peroxide	300-304	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-32	
26300283-5	2015	In addition, reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that AA decreased the activity of nrf2, NF-kappaB, AP1 and matrix metalloproteinase-3, which is stimulated by H2O2.	Hydrogen Peroxide	218-222	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	159-162	
23880762-7	2013	This increase in mitochondrial H2O2 specifically modulates MAPK signaling through the JNK/cJun pathway, whereas overexpressing Cu,Zn-SOD had no effect on any of these TCR-mediated signaling molecules.	Hydrogen Peroxide	31-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-94	
24118792-11	2013	We present a cellular model of UC and suggest a sinusoidal pattern of proliferation, which is triggered by H2 O2 -induced reactive oxygen species generation, involving an interplay between JNK activation/inactivation, p21(WAF1) , c-Fos, c-Jun/phospho-c-Jun, ATF2/phospho-ATF2, beta-catenin/TCF4-signalling, c-Myc, CDK6 and Cyclin D2, leading to driven cell cycle progression.	Hydrogen Peroxide	107-112	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	237-242	
24118792-11	2013	We present a cellular model of UC and suggest a sinusoidal pattern of proliferation, which is triggered by H2 O2 -induced reactive oxygen species generation, involving an interplay between JNK activation/inactivation, p21(WAF1) , c-Fos, c-Jun/phospho-c-Jun, ATF2/phospho-ATF2, beta-catenin/TCF4-signalling, c-Myc, CDK6 and Cyclin D2, leading to driven cell cycle progression.	Hydrogen Peroxide	107-112	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	251-256	
23129185-6	2013	Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation.	Hydrogen Peroxide	70-78	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-138	
23129185-6	2013	Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation.	Hydrogen Peroxide	70-78	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	202-207	
23129185-6	2013	Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation.	Hydrogen Peroxide	176-184	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-138	
23129185-6	2013	Further mechanistic study showed exposure of prostate cancer cells to H(2)O(2) resulted in increased phosphorylation of both JNK and c-Jun, and TAP siRNA effectively decreased H(2)O(2) -induced JNK and c-Jun phosphorylation.	Hydrogen Peroxide	176-184	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	202-207	
22413812-14	2012	Significant binding of c-Jun and CREB to the IL-32 promoter was observed in the IFNgamma + H2O2 stimulated HBE cells.	Hydrogen Peroxide	91-95	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	23-28	
22360706-0	2012	Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.	Hydrogen Peroxide	97-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-135	
22413812-18	2012	c-Jun and CREB are key transcriptional factors in IFNgamma and H2O2 induced IL-32 expression.	Hydrogen Peroxide	63-67	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5	
21814482-0	2011	Dimerumic acid inhibits SW620 cell invasion by attenuating H2O2-mediated MMP-7 expression via JNK/C-Jun and ERK/C-Fos activation in an AP-1-dependent manner.	Hydrogen Peroxide	59-63	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-103	
22146720-9	2011	Taken together, these results indicate that mangiferin attenuated H(2)O(2)-induced MMP-1 activation via inhibition of ERK and JNK pathway and AP-1.	Hydrogen Peroxide	66-74	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	142-146	
21814482-6	2011	Moreover, H2O2-triggered MMP-7 production was demonstrated via JNK/c-Jun and ERK/c-Fos activation in an activating protein 1 (AP-1)-dependent manner.	Hydrogen Peroxide	10-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-72	
21814482-7	2011	Taken together, these results suggest that DMA suppresses H2O2-induced cell invasion by inhibiting AP-1-mediated MMP-7 gene transcription via the JNK/c-Jun and ERK/c-Fos signaling pathways in SW620 human colon cancer cells.	Hydrogen Peroxide	58-62	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-155	
22102892-4	2011	Treatment with high concentrations of H2O2 (25-50 microM) for 3 h reduced insulin-stimulated Akt phosphorylation, and increased the phosphorylation of both JNK and its substrate c-Jun.	Hydrogen Peroxide	38-42	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	178-183	
19604147-5	2009	Furthermore, c-Jun Ser-63 phosphorylation was augmented in shMST3 cells, whereas JunAA (dominant-negative c-Jun) reduced H2O2 resistance, implicating an AP-1 (activator protein 1) pathway in H2O2-induced survival signalling.	Hydrogen Peroxide	121-125	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-111	
19937141-3	2009	This study examined the effects of H(2)O(2) on the activation of MAPK and AP-1 by exposing the cells to H(2)O(2) generated by either glucose oxidase or a bolus addition.	Hydrogen Peroxide	35-43	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-78	
19937141-3	2009	This study examined the effects of H(2)O(2) on the activation of MAPK and AP-1 by exposing the cells to H(2)O(2) generated by either glucose oxidase or a bolus addition.	Hydrogen Peroxide	104-112	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-78	
19937141-5	2009	H(2)O(2) increased the AP-1-DNA binding activity in these cells, where continuously generated H(2)O(2) led to an increase in mainly the c-Fos, FosB and c-Jun proteins.	Hydrogen Peroxide	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	23-27	
19937141-5	2009	H(2)O(2) increased the AP-1-DNA binding activity in these cells, where continuously generated H(2)O(2) led to an increase in mainly the c-Fos, FosB and c-Jun proteins.	Hydrogen Peroxide	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	152-157	
19937141-7	2009	However, the suppression of H(2)O(2)-induced oxidative stress by either JNK inhibitor or c-Jun specific antisense transfection was temporary in the cells exposed to glucose oxidase but not to a bolus H(2)O(2).	Hydrogen Peroxide	28-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-94	
20665665-6	2010	In addition, we found that H(2)O(2) stimulation enhanced the nuclear translocation of AP-1 and NF-kappaB subunits.	Hydrogen Peroxide	27-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-90	
19604147-5	2009	Furthermore, c-Jun Ser-63 phosphorylation was augmented in shMST3 cells, whereas JunAA (dominant-negative c-Jun) reduced H2O2 resistance, implicating an AP-1 (activator protein 1) pathway in H2O2-induced survival signalling.	Hydrogen Peroxide	191-195	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-111	
19604147-5	2009	Furthermore, c-Jun Ser-63 phosphorylation was augmented in shMST3 cells, whereas JunAA (dominant-negative c-Jun) reduced H2O2 resistance, implicating an AP-1 (activator protein 1) pathway in H2O2-induced survival signalling.	Hydrogen Peroxide	191-195	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	153-157	
19604147-5	2009	Furthermore, c-Jun Ser-63 phosphorylation was augmented in shMST3 cells, whereas JunAA (dominant-negative c-Jun) reduced H2O2 resistance, implicating an AP-1 (activator protein 1) pathway in H2O2-induced survival signalling.	Hydrogen Peroxide	191-195	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	159-178	
18385943-0	2008	The JNK/AP1/ATF2 pathway is involved in H2O2-induced acetylcholinesterase expression during apoptosis.	Hydrogen Peroxide	40-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	8-11	
19414004-3	2009	It was found that H(2)O(2)-induced apoptotic cell death in SH-SY5Y cells, which was revealed in DNA fragmentation, mitochondrial membrane potential depolarization, and activation of Akt, c-Jun N-terminal kinases (JNK) and caspase 3.	Hydrogen Peroxide	18-26	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	187-192	
18983820-4	2008	The inhibitors of hydrogen peroxide and superoxide, which were produced by mitochondria under stress, could inhibit the phosphorylation of c-Jun in XIAP knockdown cells.	Hydrogen Peroxide	18-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-144	
19038233-0	2009	trans-Resveratrol inhibits H2O2-induced adenocarcinoma gastric cells proliferation via inactivation of MEK1/2-ERK1/2-c-Jun signalling axis.	Hydrogen Peroxide	27-31	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	117-122	
18556800-0	2008	Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of AP-1 activity.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-110	
17922126-6	2008	By Western blot analysis, VK3 or H(2)O(2) was shown to induce rapid phosphorylation of extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinases (JNKs).	Hydrogen Peroxide	33-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-141	
18385943-5	2008	Taken together, our results strongly suggest that H2O2 induces AChE expression via the JNK/AP1/ ATF2 signaling pathway.	Hydrogen Peroxide	50-54	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	91-94	
18341430-6	2008	We observed that UV and H(2)O(2) induce JNK and its downstream component, c-Jun, activation in both a time- and dose-dependent manner.	Hydrogen Peroxide	24-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-79	
17566060-9	2007	Mechanistic studies revealed that Ref-1 reduction was associated with an increase of intracellular ROS levels and a marked decrease of activator protein-1 (AP-1) transcription activities in JB6P+/H2O2 cells.	Hydrogen Peroxide	196-200	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	135-154	
18154926-9	2008	In order to define the components through which NMDA or H(2)O(2) induce the final elements of these pathways, p21 and c-jun, we have performed a detailed functional analysis of c-jun and p21 promoters following plasmid transfection.	Hydrogen Peroxide	56-64	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	177-182	
17991745-6	2008	Galpha(s) repressed hydrogen peroxide-induced Bak expression by inhibiting the transcription of Bak mRNA, which resulted from the inhibition of the hydrogen peroxide-induced activation of transcription factors such as AP1, NF-kappaB, and NFAT.	Hydrogen Peroxide	20-37	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	218-221	
17991745-6	2008	Galpha(s) repressed hydrogen peroxide-induced Bak expression by inhibiting the transcription of Bak mRNA, which resulted from the inhibition of the hydrogen peroxide-induced activation of transcription factors such as AP1, NF-kappaB, and NFAT.	Hydrogen Peroxide	148-165	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	218-221	
17991745-7	2008	Moreover, Galpha(s) also inhibited the hydrogen peroxide-induced binding of AP1, NF-kappaB, and NFAT to the Bak promoter.	Hydrogen Peroxide	39-56	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-79	
17991745-9	2008	From the results, we conclude that Galpha(s) protects neuroblastoma cells from hydrogen peroxide-induced apoptosis by repressing Bak induction, which is mediated by the inhibition of the hydrogen peroxide-induced activations of AP1, NF-kappaB, and NFAT through cAMP-PKA-CREB signaling system.	Hydrogen Peroxide	187-204	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	228-231	
17566060-9	2007	Mechanistic studies revealed that Ref-1 reduction was associated with an increase of intracellular ROS levels and a marked decrease of activator protein-1 (AP-1) transcription activities in JB6P+/H2O2 cells.	Hydrogen Peroxide	196-200	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	156-160	
16836488-3	2006	Exposure of pre-confluent cells to stress conditions including IL-1beta (interleukin-1beta), H2O2 or UV irradiation resulted in marked increases in JNK activity as indicated by c-Jun phosphorylation.	Hydrogen Peroxide	93-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	177-182	
16836488-8	2006	The role of GSTA1-1 in JNK suppression was more specifically revealed in Tet-Off-inducible MEF3T3-GSTA1-1 cells in which GSTA1 overexpression significantly reduced phosphorylation of c-Jun following exposure to IL-1beta, H2O2 and UV irradiation.	Hydrogen Peroxide	221-225	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	183-188	
16356139-8	2005	Zinc deficiency-induced increases in cellular H(2)O(2) can trigger the activation of JNK and p38, leading to AP-1 activation, events that are not involved in zinc deficiency-induced apoptosis.	Hydrogen Peroxide	46-54	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	109-113	
16199533-0	2005	Hydrogen peroxide stimulates proliferation and migration of human prostate cancer cells through activation of activator protein-1 and up-regulation of the heparin affin regulatory peptide gene.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	110-129	
16199533-7	2005	The effect of HP seems to be due to the binding of Fra-1, JunD, and phospho-c-Jun to the HARP promoter.	Hydrogen Peroxide	14-16	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-81	
16199533-8	2005	These results support the notion that HARP is important for human prostate cancer cell proliferation and migration, establish the role of AP-1 in the up-regulation of HARP expression by low concentrations of HP, and characterize the AP-1 dimers involved.	Hydrogen Peroxide	208-210	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-142	
15795422-11	2005	Western blot data revealed that H2O2 upregulated phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), which was rapidly reversed by quercetin within 30 min; H2O2 activation of c-Jun was downregulated.	Hydrogen Peroxide	32-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-73	
15795422-11	2005	Western blot data revealed that H2O2 upregulated phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), which was rapidly reversed by quercetin within 30 min; H2O2 activation of c-Jun was downregulated.	Hydrogen Peroxide	202-206	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-73	
15139522-7	2004	RESULTS: TPA and H2O2 treatments strongly induced AP-1-luciferase activity as expected.	Hydrogen Peroxide	17-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	50-54	
15020252-1	2004	Hydrogen peroxide (H(2)O(2)) induces apoptosis of mesangial cells via c-Jun N-terminal kinase (JNK)-activator protein-1 (AP-1) and extracellular signal-regulated kinase (ERK)-AP-1 pathways.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75	
15020252-1	2004	Hydrogen peroxide (H(2)O(2)) induces apoptosis of mesangial cells via c-Jun N-terminal kinase (JNK)-activator protein-1 (AP-1) and extracellular signal-regulated kinase (ERK)-AP-1 pathways.	Hydrogen Peroxide	19-27	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75	
14686613-6	2003	The AP-1 complexes, induced by either IL-1 or H2O2, contained c-Fos/c-Jun and c-Fos/JunD heterodimers, but IL-1 activated AP-1 with a kinetics slower than that observed with H2O2.	Hydrogen Peroxide	174-178	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-8	
14686613-8	2003	These results indicate that H2O2 is a major mediator of IL-1-induced AP-1 activation in articular chondrocytes and that inhibition of ROS production is an effective strategy to block this IL-1-induced response.	Hydrogen Peroxide	28-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	69-73	
14686613-0	2003	Hydrogen peroxide mediates interleukin-1beta-induced AP-1 activation in articular chondrocytes: implications for the regulation of iNOS expression.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	53-57	
12057768-7	2002	Treatment of the cells with ADP, C5a and H(2)O(2) (100 microM) all increased the phosphorylation of c-Jun.	Hydrogen Peroxide	41-49	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105	
14686613-2	2003	This study aimed at elucidating the role of ROS, particularly H2O2, in mediating IL-1-induced activation of the transcription factor activator protein-1 (AP-1) in primary cultures of articular chondrocytes.	Hydrogen Peroxide	62-66	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-152	
14686613-2	2003	This study aimed at elucidating the role of ROS, particularly H2O2, in mediating IL-1-induced activation of the transcription factor activator protein-1 (AP-1) in primary cultures of articular chondrocytes.	Hydrogen Peroxide	62-66	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-158	
14686613-5	2003	The results of electrophoretic mobility shift assays showed that both IL-1 and H2O2 activated AP-1 and that inhibition of IL-1-induced ROS production abrogated AP-1 activation.	Hydrogen Peroxide	79-83	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-98	
14686613-6	2003	The AP-1 complexes, induced by either IL-1 or H2O2, contained c-Fos/c-Jun and c-Fos/JunD heterodimers, but IL-1 activated AP-1 with a kinetics slower than that observed with H2O2.	Hydrogen Peroxide	46-50	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-8	
14686613-6	2003	The AP-1 complexes, induced by either IL-1 or H2O2, contained c-Fos/c-Jun and c-Fos/JunD heterodimers, but IL-1 activated AP-1 with a kinetics slower than that observed with H2O2.	Hydrogen Peroxide	46-50	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-73	
12581340-3	2003	Hydrogen peroxide, a by-product of ROS generation, is a chemical inducer of gene expression able to activate apoptosis and to promote the antioxidant response through the activation of nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) transcription factor.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	224-243	
12581340-3	2003	Hydrogen peroxide, a by-product of ROS generation, is a chemical inducer of gene expression able to activate apoptosis and to promote the antioxidant response through the activation of nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) transcription factor.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	245-249	
12186877-2	2002	All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway.	Hydrogen Peroxide	40-57	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-154	
12186877-2	2002	All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway.	Hydrogen Peroxide	59-67	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-154	
12076508-4	2002	Short term exposure to phorbol 12-myristate 13-acetate (TPA), a phorbol ester tumour promoter, or hydrogen peroxide (H(2)O(2)) also activates AP-1 and NF-kappa B binding.	Hydrogen Peroxide	98-115	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	142-146	
12054510-7	2002	PD98059, a specific inhibitor of MEK, diminished H(2)O(2)-induced phosphorylation of c-Jun and DNA binding activity of AP-1, decreased expression of p21(WAF1/CIP1), and released the cells from G2/M arrest.	Hydrogen Peroxide	49-57	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-90	
12036993-11	2002	The results showed that the c-Jun component in the AP-1-binding complex was transiently phosphorylated during H2O2 treatment.	Hydrogen Peroxide	110-114	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-33	
12054510-0	2002	H(2)O(2)-induced AP-1 activation and its effect on p21(WAF1/CIP1)-mediated G2/M arrest in a p53-deficient human lung cancer cell.	Hydrogen Peroxide	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	17-21	
12054510-7	2002	PD98059, a specific inhibitor of MEK, diminished H(2)O(2)-induced phosphorylation of c-Jun and DNA binding activity of AP-1, decreased expression of p21(WAF1/CIP1), and released the cells from G2/M arrest.	Hydrogen Peroxide	49-57	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-123	
11796740-6	2002	At higher concentrations (mm), H(2)O(2)-stimulated a phosphorylation of c-jun.	Hydrogen Peroxide	31-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	72-77	
12053118-5	2002	Mesangial cells exposed to hydrogen peroxide undergo apoptosis through activation of the c-Jun N-terminal kinase activator protein 1 pathway.	Hydrogen Peroxide	27-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-94	
12386300-2	2002	In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1).	Hydrogen Peroxide	55-72	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-159	
12386300-2	2002	In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1).	Hydrogen Peroxide	55-72	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	161-165	
12386300-2	2002	In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1).	Hydrogen Peroxide	74-82	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-159	
12386300-2	2002	In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1).	Hydrogen Peroxide	74-82	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	161-165	
11053775-5	2000	The results show that H(2)O(2)-induced increases in egr-1, fra-1, and c-jun mRNA levels, as measured by Northern blot analysis, are time and dose dependent with the peak of the response within 2 h. Tyrosine kinase inhibitors (genistein, amino-genistein, and tyrphostin 51) significantly attenuated H(2)O(2)-induced expression of these genes and a tyrosine phosphatase inhibitor (perox-vanadate) stimulated their expression.	Hydrogen Peroxide	22-30	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75	
11278982-2	2001	Therefore, we exposed endothelial cells to hydrogen peroxide (H(2)O(2)) and observed rapid activation of JNK within 15 min that involved phosphorylation of JNK and c-Jun and induction of AP-1 DNA binding activity.	Hydrogen Peroxide	43-60	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	164-169	
11958138-3	2002	Low level of exogenous ROS H2O2(1-10 mumol/L) significantly stimulated PKB activity and c-fos/c-jun expression and cell growth, which could be abolished by antioxidant danshensu (40 mg/L).	Hydrogen Peroxide	27-31	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-99	
11053775-5	2000	The results show that H(2)O(2)-induced increases in egr-1, fra-1, and c-jun mRNA levels, as measured by Northern blot analysis, are time and dose dependent with the peak of the response within 2 h. Tyrosine kinase inhibitors (genistein, amino-genistein, and tyrphostin 51) significantly attenuated H(2)O(2)-induced expression of these genes and a tyrosine phosphatase inhibitor (perox-vanadate) stimulated their expression.	Hydrogen Peroxide	298-306	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75	
9113418-7	1997	PD98059, a specific inhibitor of MEK1, attenuated the hydrogen peroxide-induced ERKs activation and c-fos and c-jun expression.	Hydrogen Peroxide	54-71	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	110-115	
10972672-1	2000	BACKGROUND: Bioflavonoid quercetin inhibits hydrogen peroxide (H2O2)-induced apoptosis via intervention in the activator protein 1 (AP-1)-mediated apoptotic pathway.	Hydrogen Peroxide	44-61	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	111-130	
10972672-1	2000	BACKGROUND: Bioflavonoid quercetin inhibits hydrogen peroxide (H2O2)-induced apoptosis via intervention in the activator protein 1 (AP-1)-mediated apoptotic pathway.	Hydrogen Peroxide	44-61	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-136	
10972672-1	2000	BACKGROUND: Bioflavonoid quercetin inhibits hydrogen peroxide (H2O2)-induced apoptosis via intervention in the activator protein 1 (AP-1)-mediated apoptotic pathway.	Hydrogen Peroxide	63-67	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	111-130	
10972672-1	2000	BACKGROUND: Bioflavonoid quercetin inhibits hydrogen peroxide (H2O2)-induced apoptosis via intervention in the activator protein 1 (AP-1)-mediated apoptotic pathway.	Hydrogen Peroxide	63-67	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-136	
10972672-8	2000	Pretreatment with MAP kinase kinase inhibitor PD098059 or JNK-c-Jun/AP-1 inhibitor curcumin attenuated the H2O2-induced apoptosis.	Hydrogen Peroxide	107-111	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	62-67	
10972672-8	2000	Pretreatment with MAP kinase kinase inhibitor PD098059 or JNK-c-Jun/AP-1 inhibitor curcumin attenuated the H2O2-induced apoptosis.	Hydrogen Peroxide	107-111	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-72	
10814534-5	2000	Intracellular generation of hydrogen peroxide (H(2)O(2)) was also detected under serum deprivation in parental F-MEL cells, but it was suppressed in c-junAS (+) cells, in which antisense c-jun was expressed and c-Jun protein expression was inhibited as shown by Western blot.	Hydrogen Peroxide	28-45	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	149-154	
10814534-5	2000	Intracellular generation of hydrogen peroxide (H(2)O(2)) was also detected under serum deprivation in parental F-MEL cells, but it was suppressed in c-junAS (+) cells, in which antisense c-jun was expressed and c-Jun protein expression was inhibited as shown by Western blot.	Hydrogen Peroxide	28-45	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	211-216	
10400643-8	1999	Mesangial cells exposed to H2O2 undergo apoptosis via the activator protein 1 (AP-1)-dependent pathway.	Hydrogen Peroxide	27-31	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-77	
10400643-8	1999	Mesangial cells exposed to H2O2 undergo apoptosis via the activator protein 1 (AP-1)-dependent pathway.	Hydrogen Peroxide	27-31	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	79-83	
10400643-9	1999	We found that t-RA abrogated the H2O2-induced expression of c-fos/c-jun and activation of AP-1.	Hydrogen Peroxide	33-37	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71	
10400643-9	1999	We found that t-RA abrogated the H2O2-induced expression of c-fos/c-jun and activation of AP-1.	Hydrogen Peroxide	33-37	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-94	
9743233-8	1998	Moreover, phorbol 12-myristate 13-acetate, H2O2, or the combination of H2O2 and sodium orthovanadate (vanadate) activated c-Jun-activating kinase.	Hydrogen Peroxide	43-47	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-127	
9743233-8	1998	Moreover, phorbol 12-myristate 13-acetate, H2O2, or the combination of H2O2 and sodium orthovanadate (vanadate) activated c-Jun-activating kinase.	Hydrogen Peroxide	71-75	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-127	
9698606-6	1998	H2O2 also increased the expression of the early immediate genes c-jun and fra-1.	Hydrogen Peroxide	0-4	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-69	
9119028-0	1997	Mediation by arachidonic acid metabolites of the H2O2-induced stimulation of mitogen-activated protein kinases (extracellular-signal-regulated kinase and c-Jun NH2-terminal kinase).	Hydrogen Peroxide	49-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159	
9119028-2	1997	Recently, H2O2 has been reported to stimulate the activity of the mitogen-activated protein kinases (MAPKs) ERK and JNK, and the expression of the proto-oncogenes c-fos and c-jun.	Hydrogen Peroxide	10-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	173-178	
9113418-5	1997	The time courses of the hydrogen peroxide-stimulated FGFR1 tyrosine phosphorylation and ERKs activation were followed by induced expression of c-fos and c-jun.	Hydrogen Peroxide	24-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	153-158	
9113418-6	1997	Genistein, a potent inhibitor of protein tyrosine kinases, significantly blunted the hydrogen peroxide-induced FGFR1 tyrosine phosphorylation, ERKs activation and c-fos and c-jun expression.	Hydrogen Peroxide	85-102	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	173-178	
10972672-12	2000	Inhibition of ERKs by PD098059 suppressed induction of c-fos without affecting early induction of c-jun, leading to attenuated activation of AP-1 in response to H2O2.	Hydrogen Peroxide	161-165	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-145	
10972672-13	2000	CONCLUSIONS: These results suggested that (1) activation of JNK and ERKs, but not p38 kinase, is required for the H2O2-induced apoptosis; and (2) suppression of the JNK-c-Jun/AP-1 pathway and the ERK-c-Fos/AP-1 pathway is involved in the anti-apoptotic effect of quercetin.	Hydrogen Peroxide	114-118	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	169-174	
10972672-13	2000	CONCLUSIONS: These results suggested that (1) activation of JNK and ERKs, but not p38 kinase, is required for the H2O2-induced apoptosis; and (2) suppression of the JNK-c-Jun/AP-1 pathway and the ERK-c-Fos/AP-1 pathway is involved in the anti-apoptotic effect of quercetin.	Hydrogen Peroxide	114-118	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	175-179	
10972672-13	2000	CONCLUSIONS: These results suggested that (1) activation of JNK and ERKs, but not p38 kinase, is required for the H2O2-induced apoptosis; and (2) suppression of the JNK-c-Jun/AP-1 pathway and the ERK-c-Fos/AP-1 pathway is involved in the anti-apoptotic effect of quercetin.	Hydrogen Peroxide	114-118	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	206-210	
9722530-6	1998	In addition, treatment of AGS-B cells with H2O2 resulted in increased c-fos/c-jun mRNA expression and AP-1 activity, and also led to increased phosphorylation of epidermal growth factor receptor (EGFR) and Shc.	Hydrogen Peroxide	43-47	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-81	
9682214-0	1998	Bcl-2 regulates nonapoptotic signal transduction: inhibition of c-Jun N-terminal kinase (JNK) activation by IL-1 beta and hydrogen peroxide.	Hydrogen Peroxide	122-139	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-69	
9388508-4	1997	Northern blot analysis and transient transfection assays using reporter plasmids showed that H2O2 activated both AP-1 and NF-kappa B.	Hydrogen Peroxide	93-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-117	
9388508-5	1997	Downregulation of c-Jun/AP-1 using a transdominant negative mutant of c-jun, an antisense c-jun, or a pharmacologic inhibitor curcumin inhibited the H2O2-initiated apoptosis.	Hydrogen Peroxide	149-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-23	
9388508-5	1997	Downregulation of c-Jun/AP-1 using a transdominant negative mutant of c-jun, an antisense c-jun, or a pharmacologic inhibitor curcumin inhibited the H2O2-initiated apoptosis.	Hydrogen Peroxide	149-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-28	
9388508-5	1997	Downregulation of c-Jun/AP-1 using a transdominant negative mutant of c-jun, an antisense c-jun, or a pharmacologic inhibitor curcumin inhibited the H2O2-initiated apoptosis.	Hydrogen Peroxide	149-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75	
9388508-5	1997	Downregulation of c-Jun/AP-1 using a transdominant negative mutant of c-jun, an antisense c-jun, or a pharmacologic inhibitor curcumin inhibited the H2O2-initiated apoptosis.	Hydrogen Peroxide	149-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-95	
9357820-3	1997	H2O2 treatment led to increases in c-fos and c-jun mRNA levels, Jun nuclear kinase activity, and AP-1 DNA binding.	Hydrogen Peroxide	0-4	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	45-50	
9357820-6	1997	Cells expressing antisense c-jun had decreased levels of AP-1 activation and significantly increased survival after H2O2 exposure.	Hydrogen Peroxide	116-120	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32	
9113418-8	1997	Together, these results suggest that oxidants such as hydrogen peroxide stimulate tyrosine phosphorylation of receptor tyrosine kinases and these, in turn, mediate the down-stream signalling events including the recruitment of Grb2 by the receptor, activation of ERKs and induction of c-fos and c-jun expression.	Hydrogen Peroxide	54-71	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	295-300	
8910370-1	1996	We have previously reported that hydrogen peroxide, an active oxygen species and a cellular oxidant, induces c-Fos and c-Jun mRNA expression and DNA synthesis in vascular smooth muscle cells and that these events require arachidonic acid release and metabolism through the lipoxygenase pathway.	Hydrogen Peroxide	33-50	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-124	
8910370-5	1996	Hydrogen peroxide and arachidonic acid also induced the expression of c-Fos and c-Jun protein and AP-1 activity.	Hydrogen Peroxide	0-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	80-85	
8910370-6	1996	Nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway, significantly inhibited both hydrogen peroxide and arachidonic acid-stimulated c-Fos and c-Jun protein expression and AP-1 activity.	Hydrogen Peroxide	98-115	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-163	
8683110-3	1996	The present results show that Jurkat T cells acutely exposed to micromolar concentrations of H2O2 exhibit substantial increases in AP-1 binding activity and the expression of c-jun but not c-fos mRNA.	Hydrogen Peroxide	93-97	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	175-180	
8853906-3	1996	We found that both TGF-beta 1 and an oxidant, hydrogen peroxide, rapidly increase the expression of c-fos and c-jun genes and induce cell death by apoptosis; these effects are inhibited by the antioxidant N-acetylcysteine.	Hydrogen Peroxide	46-63	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	110-115	
8754823-4	1996	Gel shift assays with nuclear extracts demonstrated that H2O2 increases the binding activities of two transcription factors, NF-kappaB and AP-1, but not of Spl.	Hydrogen Peroxide	57-61	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-143	
8754823-6	1996	A supershift assay with specific antibodies against JunB, JunD, and c-Jun (Jun family) showed that the antibody against c-Jun supershifted the AP-1 complex after H2O2 treatment.	Hydrogen Peroxide	162-166	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-73	
8754823-6	1996	A supershift assay with specific antibodies against JunB, JunD, and c-Jun (Jun family) showed that the antibody against c-Jun supershifted the AP-1 complex after H2O2 treatment.	Hydrogen Peroxide	162-166	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-125	
8754823-6	1996	A supershift assay with specific antibodies against JunB, JunD, and c-Jun (Jun family) showed that the antibody against c-Jun supershifted the AP-1 complex after H2O2 treatment.	Hydrogen Peroxide	162-166	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	143-147	
8683110-4	1996	The preferential induction of c-jun by H2O2 did not represent redox stabilization of mRNA transcripts, and oxidative signals closely resembled PHA/PMA stimulation by effectively transactivating the full length c-jun promoter via the proximal jun1 tumor promoter-responsive element (TRE)-like promoter element.	Hydrogen Peroxide	39-43	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-35	
1525853-7	1992	The finding that H2O2 promotes DNA-binding of human c-jun is consistent with a similar function for PAR1/YAP1/SNQ3 and c-jun in cellular metabolism.	Hydrogen Peroxide	17-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	52-57	
7662713-11	1995	We therefore propose that superoxide anion (O2- and H2O2 generated by PQ could activate PKC and lead to induction of c-jun gene expression; on the other hand, O2- and .OH might trigger other kinase pathways to elevate ODC activity.	Hydrogen Peroxide	52-56	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	117-122	
7796393-0	1995	Transcriptional activation of the proto-oncogene c-jun by asbestos and H2O2 is directly related to increased proliferation and transformation of tracheal epithelial cells.	Hydrogen Peroxide	71-75	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	34-54	
7796393-3	1995	To examine whether asbestos or H2O2 induced transcription of c-jun, we transiently transfected HTE cells with a plasmid containing a fragment of the c-jun promoter coupled to a luciferase reporter gene.	Hydrogen Peroxide	31-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-66	
7796393-6	1995	These results demonstrate that asbestos and H2O2 activate AP-1-dependent gene transcription.	Hydrogen Peroxide	44-48	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-62	
7724734-0	1995	Heterogeneity in c-jun gene expression in normal and malignant cells exposed to either ionizing radiation or hydrogen peroxide.	Hydrogen Peroxide	109-126	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	17-22	
7724734-1	1995	We investigated the role of reactive oxygen intermediates and protein kinase C in the induction of expression of the c-jun gene in human ML-2 leukemic cells and normal human DET-551 fibroblasts by comparing the effects of exposure to either ionizing radiation or H2O2 in the presence or absence of appropriate inhibitors.	Hydrogen Peroxide	263-267	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	117-122	
7724734-2	1995	In these cell types, the radiation- and H2O2-mediated increase in c-jun mRNA levels could be prevented by pretreatment of the cells with N-acetylcysteine, an antioxidant, or H7, an inhibitor of protein kinase C and protein kinase A, but not by HA1004, a specific inhibitor of protein kinase A and G. These results suggest a role for protein kinase C and reactive oxygen intermediates in the induction of c-jun gene expression in both normal and tumor cells.	Hydrogen Peroxide	40-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71	
7724734-2	1995	In these cell types, the radiation- and H2O2-mediated increase in c-jun mRNA levels could be prevented by pretreatment of the cells with N-acetylcysteine, an antioxidant, or H7, an inhibitor of protein kinase C and protein kinase A, but not by HA1004, a specific inhibitor of protein kinase A and G. These results suggest a role for protein kinase C and reactive oxygen intermediates in the induction of c-jun gene expression in both normal and tumor cells.	Hydrogen Peroxide	40-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	404-409	
7724734-3	1995	We also investigated potential differences in c-jun gene expression induced by radiation or H2O2 in normal and tumor cells by examining steady-state c-jun mRNA levels in a number of human fibroblast, leukemia, melanoma, sarcoma and carcinoma cell types.	Hydrogen Peroxide	92-96	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	46-51	
7724734-4	1995	We observed heterogeneity in the steady-state level of c-jun mRNA in both the untreated normal and tumor cells and in such cells exposed to ionizing radiation or to H2O2.	Hydrogen Peroxide	165-169	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-60	
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	Hydrogen Peroxide	131-135	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-95	
7835407-10	1994	These results suggest that H2O2 activates protein kinase and phosphatase dependent signal transduction pathways to induce c-jun and c-fos expression which may regulate lens crystallin genes and other genes containing AP-1 binding sites.	Hydrogen Peroxide	27-31	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-127	
8814547-5	1996	Treatment with organic hydrogen peroxides mimicked UVB radiation in upregulating c-jun expression, suggesting the participation of reactive oxygen intermediates in the UVB-signaling pathway.	Hydrogen Peroxide	23-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	81-86	
8640456-2	1996	In the present study, we determined whether Ca2+ signals and the activity of protein tyrosine kinases (PTKs) were required for the induction of c-jun in Jurkat cells stimulated with cross-linked anti-T cell receptor/CD3 antibodies or exposed to oxidative stress in the form of micromolar concentrations of H2O2.	Hydrogen Peroxide	306-310	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	144-149	
8640456-7	1996	The increased expression of c-jun with H2O2 was preceded by [Ca2+]i increases and accompanied by activation of c-Jun aminoterminal kinases (JNKs), as well as increased AP-1 binding activity.	Hydrogen Peroxide	39-43	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-33	
8640456-7	1996	The increased expression of c-jun with H2O2 was preceded by [Ca2+]i increases and accompanied by activation of c-Jun aminoterminal kinases (JNKs), as well as increased AP-1 binding activity.	Hydrogen Peroxide	39-43	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	111-116	
7946382-3	1994	No c-fos mRNA was detected in HTE cells after exposure to particulates, but exposure of HTE cells to H2O2 caused striking increases in c-fos and c-jun, which preceded increases in ODC mRNA.	Hydrogen Peroxide	101-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	145-150	
7835407-0	1994	The redox active components H2O2 and N-acetyl-L-cysteine regulate expression of c-jun and c-fos in lens systems.	Hydrogen Peroxide	28-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	80-85	
7835407-3	1994	It is now demonstrated, for the first time in a lens system, that H2O2 at concentrations found in cataract patients induces expression of both c-jun and c-fos.	Hydrogen Peroxide	66-70	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	143-148	
7835407-4	1994	At optimal concentrations of H2O2, mRNA accumulation of c-jun and c-fos in the rat lenses is induced 20- and 18-fold above normal levels respectively, but with distinct kinetics.	Hydrogen Peroxide	29-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	56-61	
1525167-10	1992	In this context, H2O2 also induced c-jun expression in HL-525 cells, and this effect was inhibited by NAC.	Hydrogen Peroxide	17-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	35-40	
1525853-7	1992	The finding that H2O2 promotes DNA-binding of human c-jun is consistent with a similar function for PAR1/YAP1/SNQ3 and c-jun in cellular metabolism.	Hydrogen Peroxide	17-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-124	
1901948-3	1991	We found that expression of both c-jun and c-fos, which encode proteins that participate in formation of the AP-1 complex, is rapidly induced by two different DNA-damaging agents: UV and H2O2.	Hydrogen Peroxide	187-191	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	33-38	
34211630-4	2021	We show that TPGS induces apoptosis in K562 cells through H2O2 signaling mechanism comprising the activation of a minimal molecular cascade: the kinase JNK>the transcription factor c-JUN>the activation of BCL-only BH3 proapoptotic protein PUMA>loss of mitochondrial membrane potential (DeltaPsi m)>activation of caspase-3>chromatin condensation>fragmentation of DNA.	Hydrogen Peroxide	58-62	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	181-186