PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
24046355-3	2013	Our previous genetic studies of nephrotoxic nephritis (NTN), a form of CRGN induced by nephrotoxic serum, identified Fcgr3 and Jund as WKY genes underlying the two strongest quantitative trait loci for NTN phenotypes: Crgn1 and Crgn2, respectively.	ISONICOTINAMIDINE	55-58	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-131
30629164-9	2019	In DIO hearts as well as in neonatal rat ventricular myocytes exposed to palmitic acid, Ago2 immunoprecipitation, and luciferase assays revealed JunD as a direct target of miR-494-3p.	Palmitic Acid	73-86	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-149
24939695-10	2015	After a 30-day withdrawal from methamphetamine self-administration, however, there was mostly decreased expression of transcription factors including junD.	Methamphetamine	31-46	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-154
30746238-10	2018	However, pretreatment of NF-kappaB inhibitor BAY 11-7082 inhibited the activation of NF-kappaB under CIH condition and also significantly reduced the phosphorylation of JNK as well as c-Jun, ATF2, and JunD.	3-(4-methylphenylsulfonyl)-2-propenenitrile	45-56	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-205
22827527-0	2012	Selective up-regulation of JunD transcript and protein expression in vasopressinergic supraoptic nucleus neurones in water-deprived rats.	Water	117-122	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-31
17284934-16	2007	Resistance of Jun D protein expression to ethanol suggests that it might be a candidate for an AP-1 complex with c-Fos.	Ethanol	42-49	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17952121-0	2008	TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.	Polychlorinated Dibenzodioxins	0-4	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-81
17952121-5	2008	Here we show that TCDD treatment of rat liver oval cells leads to induction of the transcription factor JunD, resulting in transcriptional upregulation of the proto-oncogene cyclin A which finally triggers a release from contact inhibition.	Polychlorinated Dibenzodioxins	18-22	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-108
17952121-7	2008	Functional interference with AhR-, but not with ARNT, abolished TCDD-induced increase in JunD and cyclin A and prevented loss of contact inhibition.	Polychlorinated Dibenzodioxins	64-68	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-93
17952121-8	2008	In summary, we have discovered a novel AhR-dependent and probably ARNT-independent signalling pathway involving JunD and cyclin A, which mediates TCDD-induced deregulation of cell cycle control.	Polychlorinated Dibenzodioxins	146-150	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-116
20680358-6	2010	Third, capsaicin injections (physical stress) into a hind limb of the rat increased junD mRNA expression with no effect on c-fos mRNA expression, and repeated methamphetamine injections had no effect on the capsaicin-induced expression of junD mRNA.	Capsaicin	7-16	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-88
17055656-0	2007	Expression pattern of JunD after acute or chronic L-DOPA treatment: comparison with deltaFosB.	Levodopa	50-56	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-26
17055656-1	2007	In this study, we have used 6-hydroxydopamine-lesioned rats to examine changes in striatal junD and fosB/deltafosB expression induced by acute and chronic treatment with L-DOPA (5 and 15 days).	Oxidopamine	28-45	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-95
17055656-1	2007	In this study, we have used 6-hydroxydopamine-lesioned rats to examine changes in striatal junD and fosB/deltafosB expression induced by acute and chronic treatment with L-DOPA (5 and 15 days).	Levodopa	170-176	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-95
17055656-5	2007	By contrast, junD and deltafosB mRNA were both upregulated significantly above control levels after an acute injection of L-DOPA.	Levodopa	122-128	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-17
17055656-6	2007	In conclusion, this study suggests a differential expression pattern of junD and deltafosB in a rat model of L-DOPA-induced dyskinesia.	Levodopa	109-115	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-76
12670703-7	2003	The complexes formed with labeled AP1/E box oligonucleotide were reduced or supershifted with antisera to Fos family, c-Fos, Fra-2, and Jun D.	Oligonucleotides	44-59	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
16690042-0	2006	JunD attenuates phenylephrine-mediated cardiomyocyte hypertrophy by negatively regulating AP-1 transcriptional activity.	Phenylephrine	16-29	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-4
16690042-3	2006	In the present study we analyzed the mechanistic role of JunD in cardiomyocyte hypertrophy in vitro in response to alpha-adrenergic agonist phenylephrine (PE).	Phenylephrine	140-153	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-61
16690042-3	2006	In the present study we analyzed the mechanistic role of JunD in cardiomyocyte hypertrophy in vitro in response to alpha-adrenergic agonist phenylephrine (PE).	Phenylephrine	155-157	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-61
10585535-4	1999	Supershift analysis revealed that the carbachol-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	Carbachol	38-47	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Clozapine	45-54	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-154
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Haloperidol	59-70	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-154
11733514-8	2002	Truncation analysis and electromobility shift assays established the requirement for a cAMP-response element/activating transcription factor-like site in the NFLC promoter that minimally interacts with constitutively expressed cAMP-response element-binding protein and JunD as well as c-Jun which is induced by NGF in an ERK-dependent manner.	Cyclic AMP	87-91	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-273
11382404-2	2001	In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.	Ceramides	16-24	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-90
9602069-6	1998	The blockade of KA-induced proENK and proDYN mRNA levels by the pre-treatment with L-ARG was well correlated with proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, JunD, JunB, and c-Jun, as well as AP-1 and ENKCRE-2 DNA binding activities.	Arginine	83-88	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-172
9602069-9	1998	Our results suggest that L-ARG plays an important role in inhibiting KA-induced proENK or proDYN mRNA expression, and its inhibitory action may be mediated through reducing the proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, c-Jun, JunD, and JunB.	Arginine	25-30	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-242
9950818-0	1999	Polyamine depletion is associated with an increase in JunD/AP-1 activity in small intestinal crypt cells.	Polyamines	0-9	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-58
9950818-8	1999	The increased AP-1 complexes in polyamine-deficient cells were dramatically supershifted by the anti-JunD antibody but not by antibodies against c-Jun, JunB, or Fos proteins.	Polyamines	32-41	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-105
9950818-9	1999	There were significant increases in JunD mRNA and protein in DFMO-treated cells, although expression of the c-fos, c-jun, and junB genes decreased.	Eflornithine	61-65	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-40
9950818-10	1999	The increase in JunD/AP-1 activity in DFMO-treated cells was associated with a significant decrease in cell division.	Eflornithine	38-42	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-20
9950818-13	1999	These results indicate that 1) polyamine depletion is associated with an increase in AP-1 binding activity and 2) the increase in AP-1 activity in the DFMO-treated cells was primarily contributed by an increase in the JunD/AP-1.	Polyamines	31-40	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-222
9950818-13	1999	These results indicate that 1) polyamine depletion is associated with an increase in AP-1 binding activity and 2) the increase in AP-1 activity in the DFMO-treated cells was primarily contributed by an increase in the JunD/AP-1.	Eflornithine	151-155	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-222
9727025-6	1998	Transfection of a dominant negative JunD expression plasmid inhibits cAMP-mediated expression of the dopamine beta-hydroxylase promoter construct in PC12 and CATH.a cells.	Cyclic AMP	69-73	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-40
9602069-7	1998	The pre-administration with L-NAME further increased KA-induced c-jun and c-fos mRNA levels in addition to their protein product levels, although the pre-treatment with L-NAME did not affect KA-induced FosB, Fra-2, JunB, and JunD protein levels at 6 h after treatment.	NG-Nitroarginine Methyl Ester	28-34	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-229
9297634-9	1997	Using oligonucleotide competition and antibody supershift assays, we demonstrated that the cAMP-response element (CRE) motif within the V2 element interacted specifically with proteins related to cAMP-response element binding (CREB), JunB, and JunD transcription factors.	Oligonucleotides	6-21	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-248
9473635-5	1998	MK801 pretreatment produced a very strong inhibition of Fos, Jun-D and Krox-20 increases in dentate neurons but had a much smaller effect on Jun-B and c-Jun expression.	Dizocilpine Maleate	0-5	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9473635-10	1998	Conversely, the role in kindling of those genes whose expression was significantly attenuated by MK801 (Fos, Jun-D, Krox-20, trkB and BDNF) requires further examination.	Dizocilpine Maleate	97-102	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
9375664-5	1997	Gel supershift assays using transcription factor-specific antibodies revealed that p-CREB, Jun D, and a Fos family protein(s) are components of the AP-1 binding complex in untreated and lithium-treated CGC.	Lithium	186-193	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9375664-7	1997	Similar to the results obtained in CGC, p-CREB, Jun D, and Fos family proteins are present in the AP-1 binding sites in the frontal cortex and hippocampus of untreated and lithium-treated rats.	Lithium	172-179	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9297634-9	1997	Using oligonucleotide competition and antibody supershift assays, we demonstrated that the cAMP-response element (CRE) motif within the V2 element interacted specifically with proteins related to cAMP-response element binding (CREB), JunB, and JunD transcription factors.	Cyclic AMP	91-95	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-248
9134962-10	1997	In contrast, application of AMPA plus cyclothiazide induced an AP-1 transcription with contribution of Jun D, c-Fos, Fos B, c-Jun and Jun B proteins.	cyclothiazide	38-51	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9134962-8	1997	Supershift analysis with specific antibodies against the members of Fos and Jun protein families (c-Fos, Fos B, c-Jun, Jun B, Jun D) revealed that the NMDA-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	N-Methylaspartate	151-155	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7931352-6	1994	A significant increase in the levels of the mRNA encoding another IEG, junD, was also detected after haloperidol treatment.	Haloperidol	101-112	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-75
9134962-8	1997	Supershift analysis with specific antibodies against the members of Fos and Jun protein families (c-Fos, Fos B, c-Jun, Jun B, Jun D) revealed that the NMDA-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	N-Methylaspartate	151-155	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
7751931-1	1995	The effect of a single injection of caffeine on the expression of c-fos, c-jun, junB, and junD, on activator protein 1 (AP-1) and on the levels of preproenkephalin mRNA in rat striatum was studied.	Caffeine	36-44	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-94
7969116-8	1994	(i) JunD, but not CREB or other members of the Fos/Jun family, is a component of NAP binding activity in PC12 cell nuclear extracts.	N-(4-aminophenethyl)spiroperidol	81-84	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-8
8750832-1	1995	The dopamine receptor antagonist, haloperidol, produced a time-dependent differential induction of inducible transcription factors (ITFs) in rat striatal neurons: Fos, Fos B, Jun B, Jun D, Krox 20, and Krox 24, but not c-Jun, were induced in the caudate putamen and nucleus accumbens with varying time courses.	Haloperidol	34-45	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
7919180-5	1994	Twenty minutes after a single THC injection, significant increases in concentration of the mRNAs for C-FOS, C-JUN and ZIF-268 were observed in the cingulate cortex (75, 45 and 37%) and for C-FOS and ZIF-268 in the fronto-parietal cortex (60 and 64%) and caudate-putamen (81 and 32%) while JUN-D mRNA levels were not changed.	Dronabinol	30-33	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	289-294
7621509-2	1994	To investigate the role of the Jun transcription factors in neuronal differentiation, programmed neuronal cell death, and neuronal plasticity, we used phosphorothioate oligodeoxynucleotides (S-ODN) to inhibit selectively the expression of c-Jun, JunB, and JunD.	phosphorothioate oligodeoxynucleotides	151-189	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	256-260
7984056-7	1994	The mRNA levels were increased during seizures in the order of c-fos > jun-B > c-jun > jun-D in the hippocampus and jun-B > c-fos > c-jun > jun-D in the cortex, and were increased for a longer duration as well as to a greater extent than after administration of pilocarpine alone.	Pilocarpine	280-291	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
7968354-3	1994	In this report using immunocytochemical and in situ hybridization techniques we demonstrate for the first time that in addition to c-fos, pilocarpine administration increases the neuronal expression of jun-B, krox-20 and krox-24 (zif-268) but not related c-jun and jun-D genes in rat cortex and hippocampus.	Pilocarpine	138-149	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	265-270
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	48-59	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-177
1373300-2	1992	In this paper we show that 17 beta-estradiol injected into adult ovariectomized rats increases c-jun, jun-B and jun-D gene transcription in the uterus.	Estradiol	27-44	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
9831476-4	1993	Northern blot analysis of uterine RNA revealed that induction of jun-D was specific for estrogenic steroids, as progesterone and testosterone had no effect on expression of this member of the jun gene family.	Steroids	99-107	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9831476-4	1993	Northern blot analysis of uterine RNA revealed that induction of jun-D was specific for estrogenic steroids, as progesterone and testosterone had no effect on expression of this member of the jun gene family.	Progesterone	112-124	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9831476-4	1993	Northern blot analysis of uterine RNA revealed that induction of jun-D was specific for estrogenic steroids, as progesterone and testosterone had no effect on expression of this member of the jun gene family.	Testosterone	129-141	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9831476-9	1993	Slight induction of jun-D mRNA by dexamethasone was apparent, but to a much lesser extent compared to estrogen.	Dexamethasone	34-47	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8510500-4	1993	The induction of c-Jun, Jun-B, Jun-D and Fos-related proteins was prevented by administration of an N-methyl-D-aspartate receptor antagonist, which also blocked LTP induction, and by pentobarbital, which reduced but did not block LTP.	Pentobarbital	183-196	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
1421086-1	1992	The present paper describes the effect of capsaicin-induced stressful stimulus on the expression of immediate early genes (IEGs) c-fos, c-jun, junB and junD in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (ACe) using in situ hybridization.	Capsaicin	42-51	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-156
1573410-1	1992	Administration of kainate or pentylenetetrazole increased c-fos, c-jun, junB, and junD mRNA levels in rat brain in a dose-dependent manner.	Kainic Acid	18-25	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-86
1573410-1	1992	Administration of kainate or pentylenetetrazole increased c-fos, c-jun, junB, and junD mRNA levels in rat brain in a dose-dependent manner.	Pentylenetetrazole	29-47	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-86
1573410-4	1992	Adrenalectomy significantly potentiated kainate-induced increases, compared with increases caused by kainate (4 mg/kg) alone, in the hippocampal mRNA levels of c-fos and junB by 6.5-fold and of junD by twofold and tended to augment c-jun mRNA.	Kainic Acid	40-47	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-198
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	61-64	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-177
1762686-4	1991	Similar to vagotomy, application of colchicine and vinblastine on to the intact vagus nerve induced expression of c-JUN and JUN D.	Colchicine	36-46	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
1762686-4	1991	Similar to vagotomy, application of colchicine and vinblastine on to the intact vagus nerve induced expression of c-JUN and JUN D.	Vinblastine	51-62	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
34335468-6	2021	The results showed that palmitic acid stimulation induced the overexpression of JunD, impaired glucose-stimulated insulin secretion, and increased intracellular lipid accumulation of beta-cells.	Palmitic Acid	24-37	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-84
34335468-8	2021	Gene silencing of JunD reversed the lipotoxic effects induced by PA on beta-cells.	Protactinium	65-67	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-22