PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
11256818-0	2001	1H, 13C and 15N resonance assignments of the ERK2 binding domain of the MAPK phosphatase MKP-3.	Hydrogen	0-2	dual specificity phosphatase 6	Homo sapiens	89-94
11432864-4	2001	We find that ERK2/pTpY dephosphorylation by MKP3 involves an ordered, distributive mechanism in which MKP3 binds the bisphosphorylated ERK2/pTpY, dephosphorylates Tyr(P) first, dissociates and releases the monophosphorylated ERK2/pT, which is then subjected to dephosphorylation by a second MKP3, yielding the fully dephosphorylated ERK2.	Tyrosine	163-166	dual specificity phosphatase 6	Homo sapiens	44-48
11432864-4	2001	We find that ERK2/pTpY dephosphorylation by MKP3 involves an ordered, distributive mechanism in which MKP3 binds the bisphosphorylated ERK2/pTpY, dephosphorylates Tyr(P) first, dissociates and releases the monophosphorylated ERK2/pT, which is then subjected to dephosphorylation by a second MKP3, yielding the fully dephosphorylated ERK2.	Tyrosine	163-166	dual specificity phosphatase 6	Homo sapiens	102-106
11432864-4	2001	We find that ERK2/pTpY dephosphorylation by MKP3 involves an ordered, distributive mechanism in which MKP3 binds the bisphosphorylated ERK2/pTpY, dephosphorylates Tyr(P) first, dissociates and releases the monophosphorylated ERK2/pT, which is then subjected to dephosphorylation by a second MKP3, yielding the fully dephosphorylated ERK2.	Tyrosine	163-166	dual specificity phosphatase 6	Homo sapiens	102-106
11432864-5	2001	The bisphosphorylated ERK2 is a highly specific substrate for MKP3 with a k(cat)/K(m) of 3.8 x 10(6) m(-1) s(-1), which is more than 6 orders of magnitude higher than that for small molecule aryl phosphates and an ERK2-derived phosphopeptide encompassing the pTEpY motif.	Phosphates	196-206	dual specificity phosphatase 6	Homo sapiens	62-66
11284696-0	2001	Transition state analysis and requirement of Asp-262 general acid/base catalyst for full activation of dual-specificity phosphatase MKP3 by extracellular regulated kinase.	Aspartic Acid	45-48	dual specificity phosphatase 6	Homo sapiens	132-136
11284696-4	2001	Here, we investigated whether Asp-262 of MKP3 is the bona fide general acid and evaluated its contribution to the catalytic steps activated by ERK.	Aspartic Acid	30-33	dual specificity phosphatase 6	Homo sapiens	41-45
12502566-4	2002	Inhibition of ERK with the MEK inhibitor UO126, the ERK protein phosphatase MKP-3, inhibited ERK activation, but only inhibited alpha-adrenergic-induced NCX1 upregulation by 30%.	U 0126	41-46	dual specificity phosphatase 6	Homo sapiens	76-81
12105085-9	2002	MKP-1 and MKP-3 mRNAs, but not rheb mRNA, increased in the striatum, thalamus, and cortices, and in the striatum, hippocampus, and cortices, respectively, after a single methamphetamine.	Methamphetamine	170-185	dual specificity phosphatase 6	Homo sapiens	10-15
11104775-7	2001	The most important residue in the KIM sequence of MKP3 is Arg(65), which probably interacts with Asp(319) in ERK2.	Arginine	58-61	dual specificity phosphatase 6	Homo sapiens	50-54
11104775-7	2001	The most important residue in the KIM sequence of MKP3 is Arg(65), which probably interacts with Asp(319) in ERK2.	Aspartic Acid	97-100	dual specificity phosphatase 6	Homo sapiens	50-54
11256818-0	2001	1H, 13C and 15N resonance assignments of the ERK2 binding domain of the MAPK phosphatase MKP-3.	13c	4-7	dual specificity phosphatase 6	Homo sapiens	89-94
11256818-0	2001	1H, 13C and 15N resonance assignments of the ERK2 binding domain of the MAPK phosphatase MKP-3.	15n	12-15	dual specificity phosphatase 6	Homo sapiens	89-94
10702230-12	2000	Consistent with ERK stabilizing the active conformation of MKP3, the chemical chaperone dimethyl sulfoxide was able to mimic this activation.	Dimethyl Sulfoxide	88-106	dual specificity phosphatase 6	Homo sapiens	59-63
10846176-0	2000	Nitric oxide down-regulates MKP-3 mRNA levels: involvement in endothelial cell protection from apoptosis.	Nitric Oxide	0-12	dual specificity phosphatase 6	Homo sapiens	28-33
10846176-3	2000	Here we report that the endothelial cell survival factor nitric oxide (NO) down-regulated MKP-3 by destabilization of MKP-3 mRNA.	Nitric Oxide	57-69	dual specificity phosphatase 6	Homo sapiens	90-95
10846176-3	2000	Here we report that the endothelial cell survival factor nitric oxide (NO) down-regulated MKP-3 by destabilization of MKP-3 mRNA.	Nitric Oxide	57-69	dual specificity phosphatase 6	Homo sapiens	118-123
10048930-5	1999	Mutation of Asp 262, located 5.5 A distal to the active site, demonstrates it is essential for catalysis in the high-activity ERK2-dependent conformation of Pyst1 but not for the low-activity ERK2-independent form, suggesting that ERK2 induces closure of the Asp 262 loop over the active site, thereby enhancing Pyst1 catalytic efficiency.	Aspartic Acid	12-15	dual specificity phosphatase 6	Homo sapiens	312-317
10085148-5	1999	Stimulation of the cells with 12-O-tetradecanoylphorbol-13-acetate or phenylephrine induced transcription from the Glut1 promoter, which was inhibited by cotransfection with the mitogen-activated protein kinase phosphatases CL100 and MKP-3.	Tetradecanoylphorbol Acetate	30-66	dual specificity phosphatase 6	Homo sapiens	234-239
10085148-5	1999	Stimulation of the cells with 12-O-tetradecanoylphorbol-13-acetate or phenylephrine induced transcription from the Glut1 promoter, which was inhibited by cotransfection with the mitogen-activated protein kinase phosphatases CL100 and MKP-3.	Phenylephrine	70-83	dual specificity phosphatase 6	Homo sapiens	234-239
10048930-4	1999	Kinetic analysis of Pyst1 and Pyst1-CD using the substrate p-nitrophenyl phosphate (pNPP) reveals that both molecules undergo catalytic activation in the presence of recombinant inactive ERK2, switching from a low- to high-activity form.	nitrophenylphosphate	59-82	dual specificity phosphatase 6	Homo sapiens	20-25
10585426-1	1999	The mitogen-activated protein kinase phosphatase 3 (MKP3)-catalyzed hydrolysis of aryl phosphates in the absence and presence of extracellular signal-regulated kinase 2 (ERK2) was investigated in order to provide insights into the molecular basis of the ERK2-induced MKP3 activation.	aryl phosphates	82-97	dual specificity phosphatase 6	Homo sapiens	4-50
10585426-1	1999	The mitogen-activated protein kinase phosphatase 3 (MKP3)-catalyzed hydrolysis of aryl phosphates in the absence and presence of extracellular signal-regulated kinase 2 (ERK2) was investigated in order to provide insights into the molecular basis of the ERK2-induced MKP3 activation.	aryl phosphates	82-97	dual specificity phosphatase 6	Homo sapiens	52-56
10585426-2	1999	In the absence of ERK2, the MKP3-catalyzed hydrolysis of simple aryl phosphates does not display any dependence on pH, viscosity, and the nature of the leaving group.	aryl phosphates	64-79	dual specificity phosphatase 6	Homo sapiens	28-32
10585426-8	1999	Unlike simple aryl phosphates, the MKP3-catalyzed hydrolysis of bulky polycyclic substrates exhibits bell-shaped pH rate profiles in the absence of ERK2.	Phosphates	19-29	dual specificity phosphatase 6	Homo sapiens	35-39
10585426-9	1999	Furthermore, it is found that glycerol can also activate the MKP3-catalyzed reaction, increase the affinity of MKP3 for oxyanion, and restore the bell-shaped pH rate profile for the MKP3-catalyzed reaction.	Glycerol	30-38	dual specificity phosphatase 6	Homo sapiens	61-65
10585426-9	1999	Furthermore, it is found that glycerol can also activate the MKP3-catalyzed reaction, increase the affinity of MKP3 for oxyanion, and restore the bell-shaped pH rate profile for the MKP3-catalyzed reaction.	Glycerol	30-38	dual specificity phosphatase 6	Homo sapiens	111-115
10585426-9	1999	Furthermore, it is found that glycerol can also activate the MKP3-catalyzed reaction, increase the affinity of MKP3 for oxyanion, and restore the bell-shaped pH rate profile for the MKP3-catalyzed reaction.	Glycerol	30-38	dual specificity phosphatase 6	Homo sapiens	111-115
10585426-10	1999	Thus, the rate of repositioning of catalytic groups and the reorienting of the electrostatic environment in the MKP3 active site can be enhanced not only by ERK2 but also by high affinity substrates or by glycerol.	Glycerol	205-213	dual specificity phosphatase 6	Homo sapiens	112-116
10048930-4	1999	Kinetic analysis of Pyst1 and Pyst1-CD using the substrate p-nitrophenyl phosphate (pNPP) reveals that both molecules undergo catalytic activation in the presence of recombinant inactive ERK2, switching from a low- to high-activity form.	nitrophenylphosphate	59-82	dual specificity phosphatase 6	Homo sapiens	30-38
10048930-4	1999	Kinetic analysis of Pyst1 and Pyst1-CD using the substrate p-nitrophenyl phosphate (pNPP) reveals that both molecules undergo catalytic activation in the presence of recombinant inactive ERK2, switching from a low- to high-activity form.	nitrophenylphosphate	84-88	dual specificity phosphatase 6	Homo sapiens	20-25
10048930-4	1999	Kinetic analysis of Pyst1 and Pyst1-CD using the substrate p-nitrophenyl phosphate (pNPP) reveals that both molecules undergo catalytic activation in the presence of recombinant inactive ERK2, switching from a low- to high-activity form.	nitrophenylphosphate	84-88	dual specificity phosphatase 6	Homo sapiens	30-38
10048930-5	1999	Mutation of Asp 262, located 5.5 A distal to the active site, demonstrates it is essential for catalysis in the high-activity ERK2-dependent conformation of Pyst1 but not for the low-activity ERK2-independent form, suggesting that ERK2 induces closure of the Asp 262 loop over the active site, thereby enhancing Pyst1 catalytic efficiency.	Aspartic Acid	12-15	dual specificity phosphatase 6	Homo sapiens	157-162
10048930-5	1999	Mutation of Asp 262, located 5.5 A distal to the active site, demonstrates it is essential for catalysis in the high-activity ERK2-dependent conformation of Pyst1 but not for the low-activity ERK2-independent form, suggesting that ERK2 induces closure of the Asp 262 loop over the active site, thereby enhancing Pyst1 catalytic efficiency.	Aspartic Acid	259-262	dual specificity phosphatase 6	Homo sapiens	157-162
9596579-1	1998	MAP kinase phosphatase-3 (MKP-3) dephosphorylates phosphotyrosine and phosphothreonine and inactivates selectively ERK family mitogen-activated protein (MAP) kinases.	Phosphotyrosine	50-65	dual specificity phosphatase 6	Homo sapiens	0-24
9596579-1	1998	MAP kinase phosphatase-3 (MKP-3) dephosphorylates phosphotyrosine and phosphothreonine and inactivates selectively ERK family mitogen-activated protein (MAP) kinases.	Phosphotyrosine	50-65	dual specificity phosphatase 6	Homo sapiens	26-31
9596579-1	1998	MAP kinase phosphatase-3 (MKP-3) dephosphorylates phosphotyrosine and phosphothreonine and inactivates selectively ERK family mitogen-activated protein (MAP) kinases.	Phosphothreonine	70-86	dual specificity phosphatase 6	Homo sapiens	0-24
9596579-1	1998	MAP kinase phosphatase-3 (MKP-3) dephosphorylates phosphotyrosine and phosphothreonine and inactivates selectively ERK family mitogen-activated protein (MAP) kinases.	Phosphothreonine	70-86	dual specificity phosphatase 6	Homo sapiens	26-31
35439288-10	2022	A CRISPR screen identifies a synthetic lethal interaction between loss of DUSP6, an ERK negative regulator, and nelarabine treatment.	nelarabine	112-122	dual specificity phosphatase 6	Homo sapiens	74-79
34774714-5	2022	In this study, we investigated the effect of mitogen activated protein kinase (MAPK) and mitogen activated protein kinase phosphatases 1 and 3 (MKP-1 and MKP-3) on the regulation of morphine tolerance by CB2 receptor agonist.	Morphine	182-190	dual specificity phosphatase 6	Homo sapiens	154-159
34774714-6	2022	Chronic morphine treatments for 7 days reduced the protein expression of MKP-1 and MKP-3 in the spinal cord and increased the phosphorylation of p38, ERK1/2 and the level of proinflammatory mediator, such as IL-1beta, IL-6 and TNF-alpha.	Morphine	8-16	dual specificity phosphatase 6	Homo sapiens	83-88
34873301-6	2022	Flow cytometric analyses showed increased SOCS3+ and DUSP6+ T-LGL cells upon miR-181a inhibition.	mir-181a	77-85	dual specificity phosphatase 6	Homo sapiens	53-58
34837386-11	2021	CONCLUSION: Weak Dusp6 expression appears as a significant predictor of resistance of AEH/EEC to fertility-sparing treatment, with moderate predictive accuracy.	N-[3-(3-Phenylisoxazol-5-Yl)propanoyl]-L-Alpha-Glutamyl-L-Alpha-Glutamyl-Amide	90-93	dual specificity phosphatase 6	Homo sapiens	17-22
34818535-3	2021	DUSP6 mutation in Caco-2 cells enhances the epithelial feature and increases mitochondrial oxygen consumption, accompanied by altered glucose metabolism and decreased glycolysis.	Oxygen	91-97	dual specificity phosphatase 6	Homo sapiens	0-5
34803714-3	2021	BCI hydrochloride (BCI), a selective dual-specificity phosphatase 6 (DUSP6) inhibitor, is associated with multiple cellular functions, including inhibiting tumor growth and macrophage inflammation; however, its role in regulating osteoclast differentiation remains unknown.	BCI hydrochloride	0-17	dual specificity phosphatase 6	Homo sapiens	37-67
34803714-3	2021	BCI hydrochloride (BCI), a selective dual-specificity phosphatase 6 (DUSP6) inhibitor, is associated with multiple cellular functions, including inhibiting tumor growth and macrophage inflammation; however, its role in regulating osteoclast differentiation remains unknown.	BCI hydrochloride	0-17	dual specificity phosphatase 6	Homo sapiens	69-74
34803714-3	2021	BCI hydrochloride (BCI), a selective dual-specificity phosphatase 6 (DUSP6) inhibitor, is associated with multiple cellular functions, including inhibiting tumor growth and macrophage inflammation; however, its role in regulating osteoclast differentiation remains unknown.	2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	19-22	dual specificity phosphatase 6	Homo sapiens	37-67
34803714-3	2021	BCI hydrochloride (BCI), a selective dual-specificity phosphatase 6 (DUSP6) inhibitor, is associated with multiple cellular functions, including inhibiting tumor growth and macrophage inflammation; however, its role in regulating osteoclast differentiation remains unknown.	2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	19-22	dual specificity phosphatase 6	Homo sapiens	69-74
34098264-0	2021	Hydrogen sulfide exposure induces pyroptosis in the trachea of broilers via the regulatory effect of circRNA-17828/miR-6631-5p/DUSP6 crosstalk on ROS production.	Hydrogen Sulfide	0-16	dual specificity phosphatase 6	Homo sapiens	127-132
34098264-0	2021	Hydrogen sulfide exposure induces pyroptosis in the trachea of broilers via the regulatory effect of circRNA-17828/miR-6631-5p/DUSP6 crosstalk on ROS production.	Reactive Oxygen Species	146-149	dual specificity phosphatase 6	Homo sapiens	127-132
34098264-9	2021	Overexpression of miR-6631-5p or DUSP6 knockdown stimulated ROS generation and upregulated pyroptotic indicators.	Reactive Oxygen Species	60-63	dual specificity phosphatase 6	Homo sapiens	33-38
34098264-12	2021	In conclusion, circRNA-IGLL1-17828/miR-6631-5p/DUSP6 crosstalk regulated H2S-induced pyroptosis in broilers trachea via ROS generation.	Deuterium	73-76	dual specificity phosphatase 6	Homo sapiens	47-52
34098264-12	2021	In conclusion, circRNA-IGLL1-17828/miR-6631-5p/DUSP6 crosstalk regulated H2S-induced pyroptosis in broilers trachea via ROS generation.	Reactive Oxygen Species	120-123	dual specificity phosphatase 6	Homo sapiens	47-52
34774714-7	2022	Coadministration of CB2 receptor agonist AM1241 alleviated the inhibition of MKP-1 and MKP-3 by chronic morphine administration and reduced the expression of phosphorylated MAPK and proinflammatory factors.	AM 1241	41-47	dual specificity phosphatase 6	Homo sapiens	87-92
34774714-7	2022	Coadministration of CB2 receptor agonist AM1241 alleviated the inhibition of MKP-1 and MKP-3 by chronic morphine administration and reduced the expression of phosphorylated MAPK and proinflammatory factors.	Morphine	104-112	dual specificity phosphatase 6	Homo sapiens	87-92
34774714-8	2022	The effect of the CB2 receptor agonist on morphine-induced downregulation of MKP-1 and MKP-3 was reversed by the MKP-1 and MKP-3 antagonist triptolide.	Morphine	42-50	dual specificity phosphatase 6	Homo sapiens	87-92
34774714-8	2022	The effect of the CB2 receptor agonist on morphine-induced downregulation of MKP-1 and MKP-3 was reversed by the MKP-1 and MKP-3 antagonist triptolide.	Morphine	42-50	dual specificity phosphatase 6	Homo sapiens	123-128
34774714-8	2022	The effect of the CB2 receptor agonist on morphine-induced downregulation of MKP-1 and MKP-3 was reversed by the MKP-1 and MKP-3 antagonist triptolide.	triptolide	140-150	dual specificity phosphatase 6	Homo sapiens	87-92
34774714-8	2022	The effect of the CB2 receptor agonist on morphine-induced downregulation of MKP-1 and MKP-3 was reversed by the MKP-1 and MKP-3 antagonist triptolide.	triptolide	140-150	dual specificity phosphatase 6	Homo sapiens	123-128
34774714-9	2022	Our findings suggested that CB2 receptor agonist may induce the expression of MKP-1 and MKP-3 to promote MAPK dephosphorylation and reduce the production of downstream cytokine, thereby reducing morphine tolerance.	Morphine	195-203	dual specificity phosphatase 6	Homo sapiens	88-93
34711689-11	2021	However, we also found that long-term hypoxia (>12 h) induced proteasomal degradation of MKP-3 in a lactic acid-dependent manner.	Lactic Acid	100-111	dual specificity phosphatase 6	Homo sapiens	89-94
34108261-9	2021	A 4-gene signature (ASXL1, DUSP6, ERCC2, and HSPA6) correlated with CB with everolimus+/-BNC105P (AUC 86.9% (95%CI=79.2-94.7)).	Everolimus	76-86	dual specificity phosphatase 6	Homo sapiens	27-32
34970732-0	2021	Soyasaponin Ag inhibits triple-negative breast cancer progression via targeting the DUSP6/MAPK signaling.	Soyasaponin Ag	0-14	dual specificity phosphatase 6	Homo sapiens	84-89
34970732-14	2021	CONCLUSIONS: Ssa Ag inhibited TNBC progression via upregulating DUSP6 and inactivating the MAPK signaling pathway.	ssa ag	13-19	dual specificity phosphatase 6	Homo sapiens	64-69
35014672-0	2022	Overexpression of miR-375 reverses the effects of dexamethasone on the viability, migration, invasion and apoptosis of human airway epithelial cells by targeting DUSP6.	Dexamethasone	50-63	dual specificity phosphatase 6	Homo sapiens	162-167
35014672-9	2022	In the AECs (9HTE cells), Dex treatment suppressed cell viability and miR-375 expression, whereas it promoted cell apoptosis and the expression of DUSP6, the target gene of miR-375.	Dexamethasone	26-29	dual specificity phosphatase 6	Homo sapiens	147-152
35014672-10	2022	The overexpression of miR-375 reversed the effects of Dex treatment on miR-375 expression, cell viability, migration and invasion, and apoptosis-related protein expression; in turn, these effects were reversed by the overexpression of DUSP6, with the exception of miR-375 expression.	Dexamethasone	54-57	dual specificity phosphatase 6	Homo sapiens	235-240
35014672-11	2022	On the whole, the present study demonstrates that the overexpression of miR-375 counteracts the effects of Dex treatment on AEC viability, migration, invasion and apoptosis by targeting DUSP6.	Dexamethasone	107-110	dual specificity phosphatase 6	Homo sapiens	186-191
35052838-4	2022	To investigate the relationship between DUSP6 and autophagy, we exposed the ARPE-19 cell line and C57BL/6N mice to sodium iodate (NaIO3) as an oxidative stress inducer.	sodium iodate	115-128	dual specificity phosphatase 6	Homo sapiens	40-45
35008945-0	2022	Exposure of Toluene Diisocyanate Induces DUSP6 and p53 through Activation of TRPA1 Receptor.	Toluene 2,4-Diisocyanate	12-32	dual specificity phosphatase 6	Homo sapiens	41-46
32941855-6	2020	ATP and ADP enhanced phosphorylation of ERK1/2 by suppressing MKP-1 and MKP-3 expression after gamma-irradiation.	Adenosine Triphosphate	0-3	dual specificity phosphatase 6	Homo sapiens	72-77
33628737-8	2020	Signaling through the DUSP6-ERK5 pathway is modulated by MIR211 in BRAFV600E driven melanoma tumors, and this function is involved in the resistance of tumor cells to the BRAF inhibitor, Vemurafenib.	Vemurafenib	187-198	dual specificity phosphatase 6	Homo sapiens	22-27
32941855-6	2020	ATP and ADP enhanced phosphorylation of ERK1/2 by suppressing MKP-1 and MKP-3 expression after gamma-irradiation.	Adenosine Diphosphate	8-11	dual specificity phosphatase 6	Homo sapiens	72-77
31950060-11	2019	Co-immunoprecipitation (Co-IP) analyses revealed that TRIM11 interacted with DUSP6.	12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A	24-26	dual specificity phosphatase 6	Homo sapiens	77-82
32771050-9	2020	In particular, the high levels of vimentin were blunted at increasing doses of cisplatin in condition of DUSP6 over-expression while N-Cadherin contextually increased.	Cisplatin	79-88	dual specificity phosphatase 6	Homo sapiens	105-110
32376567-8	2020	Bioinformatic analysis showed that DUSP6 was the potential target gene of miR-145-5p.	mir-145-5p	74-84	dual specificity phosphatase 6	Homo sapiens	35-40
32231719-12	2020	Overexpression of DUSP6 in SKOV3 cells led to an increase in cisplatin IC50 values (P<0.05), and also markedly reduced the expression levels of phospho-ERK1/2 and CyclinD3 and to the predominance of cells in the G0/G1 phase.	Cisplatin	61-70	dual specificity phosphatase 6	Homo sapiens	18-23
31950060-11	2019	Co-immunoprecipitation (Co-IP) analyses revealed that TRIM11 interacted with DUSP6.	12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A	0-2	dual specificity phosphatase 6	Homo sapiens	77-82
30550405-5	2019	We demonstrated that docosahexenoic acid (DHA, 22:6omega-3) sensitizes the cells to the CDDP-induced inhibition of cell growth and migration by reverting CDDP effects on DNA damage and ERCC1 expression, as well as on the DUSP6 and p-ERK expressions, which regulate ERCC1 activation upwardly.	Docosahexaenoic Acids	21-40	dual specificity phosphatase 6	Homo sapiens	221-226
31553703-11	2019	This tumor suppressive effect of DUSP6 in EAC is achieved by inhibiting ERK signaling pathway.	ethyl acetoacetate	42-45	dual specificity phosphatase 6	Homo sapiens	33-38
31558717-5	2019	Through genetic code expansion, MKP3 is placed under optical control via two different approaches: (i) incorporation of a caged cysteine into the active site for controlling catalytic activity and (ii) incorporation of a caged lysine into the kinase interaction motif for controlling the protein-protein interaction between the phosphatase and its substrate.	Cysteine	128-136	dual specificity phosphatase 6	Homo sapiens	32-36
31558717-5	2019	Through genetic code expansion, MKP3 is placed under optical control via two different approaches: (i) incorporation of a caged cysteine into the active site for controlling catalytic activity and (ii) incorporation of a caged lysine into the kinase interaction motif for controlling the protein-protein interaction between the phosphatase and its substrate.	tyrosyl-lysine	227-233	dual specificity phosphatase 6	Homo sapiens	32-36
30550405-5	2019	We demonstrated that docosahexenoic acid (DHA, 22:6omega-3) sensitizes the cells to the CDDP-induced inhibition of cell growth and migration by reverting CDDP effects on DNA damage and ERCC1 expression, as well as on the DUSP6 and p-ERK expressions, which regulate ERCC1 activation upwardly.	Docosahexaenoic Acids	42-45	dual specificity phosphatase 6	Homo sapiens	221-226
30550405-5	2019	We demonstrated that docosahexenoic acid (DHA, 22:6omega-3) sensitizes the cells to the CDDP-induced inhibition of cell growth and migration by reverting CDDP effects on DNA damage and ERCC1 expression, as well as on the DUSP6 and p-ERK expressions, which regulate ERCC1 activation upwardly.	Cisplatin	88-92	dual specificity phosphatase 6	Homo sapiens	221-226
30550405-6	2019	In line, DUSP6 gene silencing prevented the effect of DHA, confirming that DHA acted on the DUSP6/p-ERK/ERCC1 repair pathways to sensitize melanoma cells to the anticancer effect of CDDP.	Docosahexaenoic Acids	54-57	dual specificity phosphatase 6	Homo sapiens	9-14
30550405-6	2019	In line, DUSP6 gene silencing prevented the effect of DHA, confirming that DHA acted on the DUSP6/p-ERK/ERCC1 repair pathways to sensitize melanoma cells to the anticancer effect of CDDP.	Docosahexaenoic Acids	75-78	dual specificity phosphatase 6	Homo sapiens	9-14
30550405-6	2019	In line, DUSP6 gene silencing prevented the effect of DHA, confirming that DHA acted on the DUSP6/p-ERK/ERCC1 repair pathways to sensitize melanoma cells to the anticancer effect of CDDP.	Docosahexaenoic Acids	75-78	dual specificity phosphatase 6	Homo sapiens	92-97
30550405-6	2019	In line, DUSP6 gene silencing prevented the effect of DHA, confirming that DHA acted on the DUSP6/p-ERK/ERCC1 repair pathways to sensitize melanoma cells to the anticancer effect of CDDP.	Cisplatin	182-186	dual specificity phosphatase 6	Homo sapiens	92-97
31164954-3	2019	Viability assays revealed a significant decrease in cell viability with pharmacological inhibition of DUSP6 using (E/Z)-BCI hydrochloride in ovarian cancer cells treated with carboplatin or paclitaxel, compared to treatment with either agent alone.	BCI hydrochloride	120-137	dual specificity phosphatase 6	Homo sapiens	102-107
31164954-3	2019	Viability assays revealed a significant decrease in cell viability with pharmacological inhibition of DUSP6 using (E/Z)-BCI hydrochloride in ovarian cancer cells treated with carboplatin or paclitaxel, compared to treatment with either agent alone.	Carboplatin	175-186	dual specificity phosphatase 6	Homo sapiens	102-107
31164954-3	2019	Viability assays revealed a significant decrease in cell viability with pharmacological inhibition of DUSP6 using (E/Z)-BCI hydrochloride in ovarian cancer cells treated with carboplatin or paclitaxel, compared to treatment with either agent alone.	Paclitaxel	190-200	dual specificity phosphatase 6	Homo sapiens	102-107
30273442-9	2019	Decreased DUSP6 expression by RNA interference in HT29 colorectal cancer cells enhanced ERK1/2 activation levels and promoted both anchorage-independent growth in soft agar as well as invasion through Matrigel.	Agar	168-172	dual specificity phosphatase 6	Homo sapiens	10-15
30577494-6	2018	Trametinib synergizes with MDM2 inhibitors through a novel DUSP6 mechanism in BRAFV600E and p53WT melanoma cells, in which DUSP6 regulation of p53 phosphorylation is mediated by ATM.	trametinib	0-10	dual specificity phosphatase 6	Homo sapiens	59-64
30552945-0	2019	The testosterone metabolite 3alpha-androstanediol inhibits oxidative stress-induced ERK phosphorylation and neurotoxicity in SH-SY5Y cells through an MKP3/DUSP6-dependent mechanism.	Testosterone	4-16	dual specificity phosphatase 6	Homo sapiens	150-154
30552945-0	2019	The testosterone metabolite 3alpha-androstanediol inhibits oxidative stress-induced ERK phosphorylation and neurotoxicity in SH-SY5Y cells through an MKP3/DUSP6-dependent mechanism.	Testosterone	4-16	dual specificity phosphatase 6	Homo sapiens	155-160
30552945-0	2019	The testosterone metabolite 3alpha-androstanediol inhibits oxidative stress-induced ERK phosphorylation and neurotoxicity in SH-SY5Y cells through an MKP3/DUSP6-dependent mechanism.	Hombreol	28-49	dual specificity phosphatase 6	Homo sapiens	150-154
30552945-0	2019	The testosterone metabolite 3alpha-androstanediol inhibits oxidative stress-induced ERK phosphorylation and neurotoxicity in SH-SY5Y cells through an MKP3/DUSP6-dependent mechanism.	Hombreol	28-49	dual specificity phosphatase 6	Homo sapiens	155-160
30552945-5	2019	In the present study, we sought to determine whether the ERK-specific phosphatase, mitogen-activated protein kinase phosphatase 3/dual specificity phosphatase 6 (MKP3/DUSP6), is involved in the cytoprotective effects of 3alpha-diol in SH-SY5Y human female neuroblastoma cells.	Androstane-3,17-diol	220-231	dual specificity phosphatase 6	Homo sapiens	162-166
30552945-5	2019	In the present study, we sought to determine whether the ERK-specific phosphatase, mitogen-activated protein kinase phosphatase 3/dual specificity phosphatase 6 (MKP3/DUSP6), is involved in the cytoprotective effects of 3alpha-diol in SH-SY5Y human female neuroblastoma cells.	Androstane-3,17-diol	220-231	dual specificity phosphatase 6	Homo sapiens	167-172
30552945-7	2019	These protective effects were significantly reduced by pre-treatment with the MKP3/DUSP6 inhibitor BCI.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	99-102	dual specificity phosphatase 6	Homo sapiens	78-82
30552945-7	2019	These protective effects were significantly reduced by pre-treatment with the MKP3/DUSP6 inhibitor BCI.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	99-102	dual specificity phosphatase 6	Homo sapiens	83-88
30552945-8	2019	In addition, H2O2 decreased expression of MKP3/DUSP6, and this was prevented by co-treatment with 3alpha-diol.	Hydrogen Peroxide	13-17	dual specificity phosphatase 6	Homo sapiens	42-46
30552945-8	2019	In addition, H2O2 decreased expression of MKP3/DUSP6, and this was prevented by co-treatment with 3alpha-diol.	Hydrogen Peroxide	13-17	dual specificity phosphatase 6	Homo sapiens	47-52
30552945-8	2019	In addition, H2O2 decreased expression of MKP3/DUSP6, and this was prevented by co-treatment with 3alpha-diol.	Androstane-3,17-diol	98-109	dual specificity phosphatase 6	Homo sapiens	42-46
30552945-8	2019	In addition, H2O2 decreased expression of MKP3/DUSP6, and this was prevented by co-treatment with 3alpha-diol.	Androstane-3,17-diol	98-109	dual specificity phosphatase 6	Homo sapiens	47-52
30552945-9	2019	These findings suggest that the protective effects of 3alpha-diol are mediated through regulation of ERK phosphorylation in neurotoxic conditions and indicate that these effects may be exerted through modulation of MKP3/DUSP6.	Androstane-3,17-diol	54-65	dual specificity phosphatase 6	Homo sapiens	215-219
30552945-9	2019	These findings suggest that the protective effects of 3alpha-diol are mediated through regulation of ERK phosphorylation in neurotoxic conditions and indicate that these effects may be exerted through modulation of MKP3/DUSP6.	Androstane-3,17-diol	54-65	dual specificity phosphatase 6	Homo sapiens	220-225
30941033-6	2019	HE4 exposure reduced Erk1/2 phosphorylation specifically in these cell populations and the effect was erased by co-incubation with a DUSP6 inhibitor, (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI).	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	150-214	dual specificity phosphatase 6	Homo sapiens	133-138
30941033-6	2019	HE4 exposure reduced Erk1/2 phosphorylation specifically in these cell populations and the effect was erased by co-incubation with a DUSP6 inhibitor, (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI).	2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	216-219	dual specificity phosphatase 6	Homo sapiens	133-138
30684529-0	2019	Hinokitiol suppresses growth of B16 melanoma by activating ERK/MKP3/proteosome pathway to downregulate survivin expression.	beta-thujaplicin	0-10	dual specificity phosphatase 6	Homo sapiens	63-67
30684529-8	2019	Hinokitiol rapidly induced ERK phosphorylation followed by a sustained dephosphorylation, which accompanied with an increase in expression of tumor suppressor MKP-3 (mitogen-activated protein kinase phosphatase-3).	beta-thujaplicin	0-10	dual specificity phosphatase 6	Homo sapiens	159-164
30684529-8	2019	Hinokitiol rapidly induced ERK phosphorylation followed by a sustained dephosphorylation, which accompanied with an increase in expression of tumor suppressor MKP-3 (mitogen-activated protein kinase phosphatase-3).	beta-thujaplicin	0-10	dual specificity phosphatase 6	Homo sapiens	166-212
30684529-9	2019	Inhibition of hinokitiol-induced ERK activation by MEK inhibitor U0126 completely blocked expression of MKP-3.	beta-thujaplicin	14-24	dual specificity phosphatase 6	Homo sapiens	104-109
30684529-9	2019	Inhibition of hinokitiol-induced ERK activation by MEK inhibitor U0126 completely blocked expression of MKP-3.	U 0126	65-70	dual specificity phosphatase 6	Homo sapiens	104-109
30684529-10	2019	More importantly, inhibition of MKP-3 activity by NSC 95397 significantly inhibited hinokitiol-induced ERK dephosphorylation, ubiquitination and downregulation of survivin.	beta-thujaplicin	84-94	dual specificity phosphatase 6	Homo sapiens	32-37
30684529-11	2019	These results suggested that hinokitiol inhibited growth of B16-F10 melanoma through downregulation of survivin by activating ERK/MKP-3/proteosome pathway.	beta-thujaplicin	29-39	dual specificity phosphatase 6	Homo sapiens	130-135
30577494-6	2018	Trametinib synergizes with MDM2 inhibitors through a novel DUSP6 mechanism in BRAFV600E and p53WT melanoma cells, in which DUSP6 regulation of p53 phosphorylation is mediated by ATM.	trametinib	0-10	dual specificity phosphatase 6	Homo sapiens	123-128
29375309-5	2017	Stimulation with the specific P2X7 agonist, BzATP, or epidermal growth factor (EGF) (positive control for ERK activation) regulates the levels of DUSP6 in a time dependent manner.	3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate	44-49	dual specificity phosphatase 6	Homo sapiens	146-151
30577494-0	2018	ATM Dependent DUSP6 Modulation of p53 Involved in Synergistic Targeting of MAPK and p53 Pathways with Trametinib and MDM2 Inhibitors in Cutaneous Melanoma.	trametinib	102-112	dual specificity phosphatase 6	Homo sapiens	14-19
30577494-4	2018	In addition, DUSP6 phosphatase involvement was indicated by downregulation of its mRNA and protein following pERK reduction by trametinib.	trametinib	127-137	dual specificity phosphatase 6	Homo sapiens	13-18
30577494-5	2018	Furthermore, suppression of DUSP6 by siRNA, or inhibition with the small molecule inhibitor, BCI, at a dose without cytotoxicity, potentiated the effect of MDM2 inhibitors through increased ATM-dependent p53 phosphorylation, as demonstrated by complete reversal with the ATM inhibitor, KU55933.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	286-293	dual specificity phosphatase 6	Homo sapiens	28-33
29745428-4	2018	Upon exposure of purified PMBCs to HE4, osteopontin (OPN) and dual-specificity phosphatase 6 (DUSP6) emerged as the most suppressed and up-regulated genes, respectively.	pmbcs	26-31	dual specificity phosphatase 6	Homo sapiens	62-92
29745428-4	2018	Upon exposure of purified PMBCs to HE4, osteopontin (OPN) and dual-specificity phosphatase 6 (DUSP6) emerged as the most suppressed and up-regulated genes, respectively.	pmbcs	26-31	dual specificity phosphatase 6	Homo sapiens	94-99
30260967-9	2018	To further elucidate the mechanism(s) underlying GPx3-medited suppression of tumor proliferation, we next examined the effect of GPx3-mediated redox signaling on the ROS-MKP3-extracellular signal-regulated kinase (Erk)-NF-kappaB-cyclin B1 pathway and found that GPx3 strongly suppressed activation of the Erk-NF-kappaB-cyclin B1 signaling cascade by protecting MKP3 (an Erk-specific phosphatase) from the effects of ROS.	Reactive Oxygen Species	166-169	dual specificity phosphatase 6	Homo sapiens	170-174
29375309-6	2017	Both agonists promote a decline in DUSP6 protein, reaching minimal levels after 30 min yet recovering to basal levels after 1 h. The initial loss of protein occurs through proteasomal degradation, as confirmed in experiments with the proteasome inhibitor, MG-132.	Magnesium	256-258	dual specificity phosphatase 6	Homo sapiens	35-40
29375309-7	2017	Studies carried out with Actinomycin D demonstrated that the enhanced transcription of the Dusp6 gene is responsible for recovering the DUSP6 protein levels.	Dactinomycin	25-38	dual specificity phosphatase 6	Homo sapiens	91-96
29375309-7	2017	Studies carried out with Actinomycin D demonstrated that the enhanced transcription of the Dusp6 gene is responsible for recovering the DUSP6 protein levels.	Dactinomycin	25-38	dual specificity phosphatase 6	Homo sapiens	136-141
29050982-0	2018	Pharmacological inhibition of DUSP6 suppresses gastric cancer growth and metastasis and overcomes cisplatin resistance.	Cisplatin	98-107	dual specificity phosphatase 6	Homo sapiens	30-35
29050982-6	2018	(E/Z)-BCI hydrochloride (BCI), a DUSP6 small molecule inhibitor, increased the activity of ERK but interestingly decreased the expression of ERK response genes in BGC823, SGC7901 and CDDP-resistant SGC7901/DDP cells.	BCI hydrochloride	6-23	dual specificity phosphatase 6	Homo sapiens	33-38
29050982-6	2018	(E/Z)-BCI hydrochloride (BCI), a DUSP6 small molecule inhibitor, increased the activity of ERK but interestingly decreased the expression of ERK response genes in BGC823, SGC7901 and CDDP-resistant SGC7901/DDP cells.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	6-9	dual specificity phosphatase 6	Homo sapiens	33-38
29050982-10	2018	In summary, our findings indicated that disruption of DUSP6 by BCI enhanced CDDP-induced cell death and apoptosis in GC may partly through ERK and DDR pathways.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	63-66	dual specificity phosphatase 6	Homo sapiens	54-59
29050982-10	2018	In summary, our findings indicated that disruption of DUSP6 by BCI enhanced CDDP-induced cell death and apoptosis in GC may partly through ERK and DDR pathways.	Cisplatin	76-80	dual specificity phosphatase 6	Homo sapiens	54-59
28876465-5	2018	Additional molecular studies revealed that B2G2-induced cell death was mediated mainly through ROS-induced sustained activation of ERK1/2, which was due to inhibition of MAP kinase phosphatase (MKP) activity as over-expression of MKP3 in LNCaP cells conferred significant protection against B2G2-induced cell death.	Reactive Oxygen Species	95-98	dual specificity phosphatase 6	Homo sapiens	230-234
27422819-9	2016	Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH to levels comparable with ERK phosphorylated in the presence of FSH.	Threonine	77-80	dual specificity phosphatase 6	Homo sapiens	39-43
28611044-6	2017	MK-4166 decreased induction and suppressive effects of Tregsin vitro In human TIL cultures, MK-4166 induced phosphorylation of NFkappaB and increased expression of dual specificity phosphatase 6 (DUSP6), indicating that MK-4166 activated downstream NFkappaB and Erk signaling pathways.	mk-4166	0-7	dual specificity phosphatase 6	Homo sapiens	164-194
28611044-6	2017	MK-4166 decreased induction and suppressive effects of Tregsin vitro In human TIL cultures, MK-4166 induced phosphorylation of NFkappaB and increased expression of dual specificity phosphatase 6 (DUSP6), indicating that MK-4166 activated downstream NFkappaB and Erk signaling pathways.	mk-4166	0-7	dual specificity phosphatase 6	Homo sapiens	196-201
28611044-6	2017	MK-4166 decreased induction and suppressive effects of Tregsin vitro In human TIL cultures, MK-4166 induced phosphorylation of NFkappaB and increased expression of dual specificity phosphatase 6 (DUSP6), indicating that MK-4166 activated downstream NFkappaB and Erk signaling pathways.	mk-4166	92-99	dual specificity phosphatase 6	Homo sapiens	164-194
28611044-6	2017	MK-4166 decreased induction and suppressive effects of Tregsin vitro In human TIL cultures, MK-4166 induced phosphorylation of NFkappaB and increased expression of dual specificity phosphatase 6 (DUSP6), indicating that MK-4166 activated downstream NFkappaB and Erk signaling pathways.	mk-4166	92-99	dual specificity phosphatase 6	Homo sapiens	196-201
28989118-8	2017	Cultured myotubes express both MKPs, and incubation with dexamethasone (Dex) mimicked the in vivo expression pattern of DUSP5 and DUSP6 caused by exercise.	Dexamethasone	57-70	dual specificity phosphatase 6	Homo sapiens	130-135
28989118-8	2017	Cultured myotubes express both MKPs, and incubation with dexamethasone (Dex) mimicked the in vivo expression pattern of DUSP5 and DUSP6 caused by exercise.	Dexamethasone	72-75	dual specificity phosphatase 6	Homo sapiens	130-135
28496200-8	2017	We also showed that dual-specificity phosphatase 6 (DUSP6) is a novel target of miR-200a-3p and regulates resistance to 5-FU.	Fluorouracil	120-124	dual specificity phosphatase 6	Homo sapiens	20-50
28496200-8	2017	We also showed that dual-specificity phosphatase 6 (DUSP6) is a novel target of miR-200a-3p and regulates resistance to 5-FU.	Fluorouracil	120-124	dual specificity phosphatase 6	Homo sapiens	52-57
28161489-5	2017	Bortezomib decreases ERK1/2 phosphorylation whereas induces the accumulation of MKP-3 - a specific ERK1/2 MAP kinase phosphatase - in time and concentration dependent manner (1.5-32h; 0.25-1nM).	Bortezomib	0-10	dual specificity phosphatase 6	Homo sapiens	80-85
28161489-5	2017	Bortezomib decreases ERK1/2 phosphorylation whereas induces the accumulation of MKP-3 - a specific ERK1/2 MAP kinase phosphatase - in time and concentration dependent manner (1.5-32h; 0.25-1nM).	2-Bromo-3-(4-Bromophenyl)-4-Hydroxy-6-Oxo-6,7-Dihydrothieno[2,3-B]pyridine-5-Carbonitrile	179-182	dual specificity phosphatase 6	Homo sapiens	80-85
28161489-9	2017	Consistent with FOXO1 dephosphorylation/activation, p21 mRNA expression is increased by Bortezomib in a MKP-3-dependent way.	Bortezomib	88-98	dual specificity phosphatase 6	Homo sapiens	104-109
28161489-11	2017	It is concluded that in vGPCR cells, Bortezomib decreases ERK1/2 and FOXO1 phosphorylation through MKP-3 accumulation, leading ERK1/2 deactivation and FOXO1 activation respectively and, consequently, to cell proliferation inhibition, p21 induction and VEGF repression.	Bortezomib	37-47	dual specificity phosphatase 6	Homo sapiens	99-104
28350009-0	2017	Activation of ERK1/2 Causes Pazopanib Resistance via Downregulation of DUSP6 in Synovial Sarcoma Cells.	pazopanib	28-37	dual specificity phosphatase 6	Homo sapiens	71-76
28350009-9	2017	In the pazopanib-resistant clones, dual specificity phosphatase 6 (DUSP6) was downregulated.	pazopanib	7-16	dual specificity phosphatase 6	Homo sapiens	35-65
28350009-9	2017	In the pazopanib-resistant clones, dual specificity phosphatase 6 (DUSP6) was downregulated.	pazopanib	7-16	dual specificity phosphatase 6	Homo sapiens	67-72
28350009-10	2017	Inhibition of DUSP6 expression in parental HS-SY-II cells partially recapitulated acquired pazopanib resistance.	pazopanib	91-100	dual specificity phosphatase 6	Homo sapiens	14-19
28350009-11	2017	Acquired pazopanib resistance in SS was associated with activation of ERK1/2 through downregulation of DUSP6 expression.	pazopanib	9-18	dual specificity phosphatase 6	Homo sapiens	103-108
27422819-9	2016	Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH to levels comparable with ERK phosphorylated in the presence of FSH.	Threonine	77-80	dual specificity phosphatase 6	Homo sapiens	45-50
27422819-9	2016	Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH to levels comparable with ERK phosphorylated in the presence of FSH.	Tyrosine	86-89	dual specificity phosphatase 6	Homo sapiens	39-43
27422819-9	2016	Treatment with MAP kinase phosphatase (MKP3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH to levels comparable with ERK phosphorylated in the presence of FSH.	Tyrosine	86-89	dual specificity phosphatase 6	Homo sapiens	45-50
27191743-11	2016	Clinical evidences suggested that genes affected by CAPE treatment (CTNNB1, RELA, FZD5, DVL3, MAPK9, SNAl1, ROR2, SMAD4, NFKBIA, DUSP6, and PLCB3) correlate with the aggressiveness of PCa.	caffeic acid phenethyl ester	52-56	dual specificity phosphatase 6	Homo sapiens	129-134
27216486-10	2016	In BD fibroblasts, DUSP6 knockdown reversed the BD rhythm phenotype, restoring the ability of lithium to increase amplitude in these cells.	Lithium	94-101	dual specificity phosphatase 6	Homo sapiens	19-24
26379838-5	2015	Down regulation of DUSP6 in MDA-MB-231 cells suppressed the cell proliferation as investigated by MTT assay and colony form assay.	monooxyethylene trimethylolpropane tristearate	98-101	dual specificity phosphatase 6	Homo sapiens	19-24
26435497-10	2015	Inhibition of the ERK1/2 pathway by PD98059 and FR180204 resulted in a decrease in DUSP6 and DUSP7 expression, both in resting and LPS-stimulated microglia.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	36-43	dual specificity phosphatase 6	Homo sapiens	83-88
26435497-13	2015	BCI, an inhibitor of DUSP6, increased the phosphorylation of ERK1/2.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	0-3	dual specificity phosphatase 6	Homo sapiens	21-26
25970467-5	2015	Microarray expression profiling of normal versus starved H295R cells revealed fourteen differentially expressed genes; HSD3B2, HSD3B1, CYP21A2, RARB, ASS1, CFI, ASCL1 and ENC1 play a role in steroid and energy metabolism and ANGPTL1, PLK2, DUSP6, DUSP10 and FREM2 are involved in signal transduction.	Steroids	191-198	dual specificity phosphatase 6	Homo sapiens	240-245
25846811-12	2015	Importantly, metformin induced ERK activation by suppressing the protein levels of dual specificity phosphatase 6, a negative regulator of ERK.	Metformin	13-22	dual specificity phosphatase 6	Homo sapiens	83-113
23419500-0	2013	Dual-specificity phosphatase 6 (Dusp6), a negative regulator of FGF2/ERK1/2 signaling, enhances 17beta-estradiol-induced cell growth in endometrial adenocarcinoma cell.	Estradiol	96-112	dual specificity phosphatase 6	Homo sapiens	0-30
24704509-4	2014	Conformation-selective ligands are also able to modulate Erk2"s ability to allosterically activate the MAPK phosphatase DUSP6, highlighting how ATP-competitive ligands can control noncatalytic kinase functions.	Adenosine Triphosphate	144-147	dual specificity phosphatase 6	Homo sapiens	120-125
23921636-3	2013	Binding studies revealed PR-B interacts with dual-specificity phosphatase 6 (DUSP6) via the CD domain.	Cadmium	92-94	dual specificity phosphatase 6	Homo sapiens	45-75
23921636-3	2013	Binding studies revealed PR-B interacts with dual-specificity phosphatase 6 (DUSP6) via the CD domain.	Cadmium	92-94	dual specificity phosphatase 6	Homo sapiens	77-82
25499223-6	2014	Although DUSP6 protein was degraded by B-RafV600E-induced reactive oxygen species (ROS), thyroid-stimulating hormone (TSH) stabilized DUSP6 protein by increasing Mn superoxide dismutase expression and inhibited B-RafV600E-induced senescence.	Reactive Oxygen Species	58-81	dual specificity phosphatase 6	Homo sapiens	9-14
25499223-6	2014	Although DUSP6 protein was degraded by B-RafV600E-induced reactive oxygen species (ROS), thyroid-stimulating hormone (TSH) stabilized DUSP6 protein by increasing Mn superoxide dismutase expression and inhibited B-RafV600E-induced senescence.	Reactive Oxygen Species	83-86	dual specificity phosphatase 6	Homo sapiens	9-14
23246965-0	2014	DeltaNp63alpha regulates Erk signaling via MKP3 to inhibit cancer metastasis.	deltanp63alpha	0-14	dual specificity phosphatase 6	Homo sapiens	43-47
23246965-4	2014	We show that DeltaNp63alpha regulates extracellular signal-regulated protein kinases 1 and 2 (Erk1/2) activity via MKP3 in both cancer and non-transformed cells.	deltanp63alpha	13-27	dual specificity phosphatase 6	Homo sapiens	115-119
24260056-6	2013	Treatment with 5-aza-2"-deoxycytidine restored DUSP6 expression in the two ESCC cell lines, and the expression varied according to the drug concentration.	Decitabine	15-37	dual specificity phosphatase 6	Homo sapiens	47-52
23419500-0	2013	Dual-specificity phosphatase 6 (Dusp6), a negative regulator of FGF2/ERK1/2 signaling, enhances 17beta-estradiol-induced cell growth in endometrial adenocarcinoma cell.	Estradiol	96-112	dual specificity phosphatase 6	Homo sapiens	32-37
23419500-6	2013	In Dusp6 forced-expression cells, 17beta-estradiol stimulation increased the cell growth by all most threefolds.	Estradiol	34-50	dual specificity phosphatase 6	Homo sapiens	3-8
23419500-9	2013	Dusp6 functions as a negative regulator of FGF2/ERK1/2 signaling but enhances the growth and 17beta-estradiol-induced cell growth in endometrial adenocarcinoma cell.	Estradiol	93-109	dual specificity phosphatase 6	Homo sapiens	0-5
21996734-8	2012	DUSP6 overexpression prevented cisplatin induction of both ERCC1 and XPF, resulting in increased sensitivity to cisplatin.	Cisplatin	31-40	dual specificity phosphatase 6	Homo sapiens	0-5
22155192-2	2012	Previously, we reported a positive association between the functional Leu114Val polymorphism (rs2279574) in DUSP6 and bipolar disorder.	leu114val	70-79	dual specificity phosphatase 6	Homo sapiens	108-113
22155192-7	2012	We also investigated the functions of the functional SNPs" positive associations and found that Leu114Val (rs2279574; T/G) and Ser144Ala (rs770087; T/G) mutations in DUSP6 proteins reduced lithium-induced ERK1/2 phosphorylation in vitro, implicating the dominant active functions.	leu114val	96-105	dual specificity phosphatase 6	Homo sapiens	166-171
22155192-7	2012	We also investigated the functions of the functional SNPs" positive associations and found that Leu114Val (rs2279574; T/G) and Ser144Ala (rs770087; T/G) mutations in DUSP6 proteins reduced lithium-induced ERK1/2 phosphorylation in vitro, implicating the dominant active functions.	Lithium	189-196	dual specificity phosphatase 6	Homo sapiens	166-171
22155192-8	2012	Thus, DUSP6 may not only play important roles in the pathogenesis of bipolar disorder, particularly in women, but also affect the therapeutic response to lithium through modulating lithium"s effects on intracellular signaling.	Lithium	154-161	dual specificity phosphatase 6	Homo sapiens	6-11
22155192-8	2012	Thus, DUSP6 may not only play important roles in the pathogenesis of bipolar disorder, particularly in women, but also affect the therapeutic response to lithium through modulating lithium"s effects on intracellular signaling.	Lithium	181-188	dual specificity phosphatase 6	Homo sapiens	6-11
23261984-4	2013	Here we analyzed MKP-3 expression in MA-10 Leydig cells and demonstrated that LH receptor (LHR) activation with human gonadotropin hormone (hCG) and an analog of its second messenger, 8Br-cAMP, up-regulates MKP-3 by transcriptional and post-translational mechanisms.	8-Bromo Cyclic Adenosine Monophosphate	184-192	dual specificity phosphatase 6	Homo sapiens	207-212
23063941-4	2012	In this study, we examined the effects of haloperidol on DUSP6 expression related to DNA methylation changes.	Haloperidol	42-53	dual specificity phosphatase 6	Homo sapiens	57-62
23063941-5	2012	MAIN METHODS: The effects of haloperidol and 5-azacytidine, a demethylating agent, on expression and methylation of DUSP6 were quantitatively measured in MIA PaCa-2 human pancreatic carcinoma cells, in which DUSP6 expression is suppressed due to intronic hypermethylation.	Haloperidol	29-40	dual specificity phosphatase 6	Homo sapiens	116-121
23063941-5	2012	MAIN METHODS: The effects of haloperidol and 5-azacytidine, a demethylating agent, on expression and methylation of DUSP6 were quantitatively measured in MIA PaCa-2 human pancreatic carcinoma cells, in which DUSP6 expression is suppressed due to intronic hypermethylation.	Azacitidine	45-58	dual specificity phosphatase 6	Homo sapiens	116-121
23063941-5	2012	MAIN METHODS: The effects of haloperidol and 5-azacytidine, a demethylating agent, on expression and methylation of DUSP6 were quantitatively measured in MIA PaCa-2 human pancreatic carcinoma cells, in which DUSP6 expression is suppressed due to intronic hypermethylation.	Azacitidine	45-58	dual specificity phosphatase 6	Homo sapiens	208-213
23063941-7	2012	KEY FINDINGS: Haloperidol increased DUSP6 expression in a concentration-dependent manner and inhibited MIA PaCa-2 cell proliferation; effects were comparable to those of 5-azacytidine.	Haloperidol	14-25	dual specificity phosphatase 6	Homo sapiens	36-41
23063941-9	2012	Pyrosequencing methylation analysis confirmed the intronic hypermethylation of DUSP6 in MIA PaCa-2 and revealed that haloperidol and 5-azcytidine induced demethylation of CpG sequences in this region.	Haloperidol	117-128	dual specificity phosphatase 6	Homo sapiens	79-84
23063941-9	2012	Pyrosequencing methylation analysis confirmed the intronic hypermethylation of DUSP6 in MIA PaCa-2 and revealed that haloperidol and 5-azcytidine induced demethylation of CpG sequences in this region.	5-azcytidine	133-145	dual specificity phosphatase 6	Homo sapiens	79-84
23063941-10	2012	SIGNIFICANCE: Haloperidol induced DUSP6 expression related to intronic demethylation and inhibited MIA PaCa-2 cell proliferation, which suggests demethylating activity and anti-cancer effects of haloperidol.	Haloperidol	14-25	dual specificity phosphatase 6	Homo sapiens	34-39
23063941-10	2012	SIGNIFICANCE: Haloperidol induced DUSP6 expression related to intronic demethylation and inhibited MIA PaCa-2 cell proliferation, which suggests demethylating activity and anti-cancer effects of haloperidol.	Haloperidol	195-206	dual specificity phosphatase 6	Homo sapiens	34-39
23108049-5	2012	Expression of shDUSP6 inhibited 5"-FU-induced cell death, whereas overexpression of DUSP6 increased susceptibility to 5"-FU.	Fluorouracil	32-37	dual specificity phosphatase 6	Homo sapiens	16-21
23108049-6	2012	5"-FU treatment dephosphorylated ERK in a DUSP6-dependent manner, resulting in destabilization of Bcl-2 and stabilization of Bad.	Fluorouracil	0-5	dual specificity phosphatase 6	Homo sapiens	42-47
23023500-5	2012	DUSP6 repression using miR-181a or specific siRNA and DUSP6 inhibition by the allosteric inhibitor (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one improved CD4(+) T cell responses, as seen by increased expression of activation markers, improved proliferation and supported preferential T helper type 1 cell differentiation.	mir-181a	23-31	dual specificity phosphatase 6	Homo sapiens	0-5
23023500-5	2012	DUSP6 repression using miR-181a or specific siRNA and DUSP6 inhibition by the allosteric inhibitor (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one improved CD4(+) T cell responses, as seen by increased expression of activation markers, improved proliferation and supported preferential T helper type 1 cell differentiation.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	99-163	dual specificity phosphatase 6	Homo sapiens	0-5
23023500-5	2012	DUSP6 repression using miR-181a or specific siRNA and DUSP6 inhibition by the allosteric inhibitor (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one improved CD4(+) T cell responses, as seen by increased expression of activation markers, improved proliferation and supported preferential T helper type 1 cell differentiation.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	99-163	dual specificity phosphatase 6	Homo sapiens	54-59
21996734-8	2012	DUSP6 overexpression prevented cisplatin induction of both ERCC1 and XPF, resulting in increased sensitivity to cisplatin.	Cisplatin	112-121	dual specificity phosphatase 6	Homo sapiens	0-5
21454500-1	2011	MAPK phosphatase 3 (MKP3) is highly specific for ERK1/2 inactivation via dephosphorylation of both phosphotyrosine and phosphothreonine critical for enzymatic activation.	Phosphotyrosine	99-114	dual specificity phosphatase 6	Homo sapiens	0-18
22169769-8	2012	We identified a single gene DUSP6, whose expression was associated with sensitivity to GSK1120212 and lack of expression associated with resistance irrelevant of RAF/RAS status.	trametinib	87-97	dual specificity phosphatase 6	Homo sapiens	28-33
22277373-6	2012	The expression of MKP3 increased in a cisplatin-resistant NSCLC cell line and lung xenografts.	Cisplatin	38-47	dual specificity phosphatase 6	Homo sapiens	18-22
22848708-4	2012	Here, we address the association between MKP-3 and endothelial Nitric oxide (NO) formation under ischemia/reperfusion (IS/RP) condition.	Nitric Oxide	63-75	dual specificity phosphatase 6	Homo sapiens	41-46
22848708-11	2012	Finally, Salvianolic acid A (SalA) markedly attenuated induction of MKP-3 and inhibition of eNOS expression and NO formation under endothelial IS/RP condition.	salvianolic acid A	9-27	dual specificity phosphatase 6	Homo sapiens	68-73
22848708-11	2012	Finally, Salvianolic acid A (SalA) markedly attenuated induction of MKP-3 and inhibition of eNOS expression and NO formation under endothelial IS/RP condition.	salvianolic acid A	29-33	dual specificity phosphatase 6	Homo sapiens	68-73
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphotyrosine	120-135	dual specificity phosphatase 6	Homo sapiens	0-30
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphotyrosine	120-135	dual specificity phosphatase 6	Homo sapiens	32-37
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphotyrosine	120-135	dual specificity phosphatase 6	Homo sapiens	96-101
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphothreonine	140-156	dual specificity phosphatase 6	Homo sapiens	0-30
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphothreonine	140-156	dual specificity phosphatase 6	Homo sapiens	32-37
21499306-1	2011	Dual-specificity phosphatase 6 (DUSP6, mitogen-activated protein kinase (MAPK) phosphatase 3 or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on extracellular signal-regulated kinase (ERK1/2; MAPK1/2) to inactivate the ERK1/2 kinase.	Phosphothreonine	140-156	dual specificity phosphatase 6	Homo sapiens	96-101
21499306-8	2011	Importantly, DUSP6 overexpression increased resistance to cisplatin-mediated cell death in vitro and in vivo.	Cisplatin	58-67	dual specificity phosphatase 6	Homo sapiens	13-18
21454500-1	2011	MAPK phosphatase 3 (MKP3) is highly specific for ERK1/2 inactivation via dephosphorylation of both phosphotyrosine and phosphothreonine critical for enzymatic activation.	Phosphotyrosine	99-114	dual specificity phosphatase 6	Homo sapiens	20-24
21454500-1	2011	MAPK phosphatase 3 (MKP3) is highly specific for ERK1/2 inactivation via dephosphorylation of both phosphotyrosine and phosphothreonine critical for enzymatic activation.	Phosphothreonine	119-135	dual specificity phosphatase 6	Homo sapiens	0-18
21454500-1	2011	MAPK phosphatase 3 (MKP3) is highly specific for ERK1/2 inactivation via dephosphorylation of both phosphotyrosine and phosphothreonine critical for enzymatic activation.	Phosphothreonine	119-135	dual specificity phosphatase 6	Homo sapiens	20-24
21454500-2	2011	Here, we show that MKP3 is able to effectively dephosphorylate the phosphotyrosine, but not phosphothreonine, in the activation loop of p38alpha in vitro and in intact cells.	Phosphotyrosine	67-82	dual specificity phosphatase 6	Homo sapiens	19-23
21454500-2	2011	Here, we show that MKP3 is able to effectively dephosphorylate the phosphotyrosine, but not phosphothreonine, in the activation loop of p38alpha in vitro and in intact cells.	Phosphothreonine	92-108	dual specificity phosphatase 6	Homo sapiens	19-23
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphotyrosine	85-100	dual specificity phosphatase 6	Homo sapiens	45-50
21300799-9	2011	Indeed, Dusp6 overexpression as well as incubation with UO126 produced an increase in AMPA receptor-induced inward currents and cytosolic calcium overload.	Calcium	138-145	dual specificity phosphatase 6	Homo sapiens	8-13
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphotyrosine	85-100	dual specificity phosphatase 6	Homo sapiens	52-56
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphotyrosine	85-100	dual specificity phosphatase 6	Homo sapiens	61-66
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphothreonine	105-121	dual specificity phosphatase 6	Homo sapiens	45-50
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphothreonine	105-121	dual specificity phosphatase 6	Homo sapiens	52-56
20638106-1	2010	OBJECTIVE: Dual-specificity phosphatase six (DUSP6, MKP3, or PYST1) dephosphorylates phosphotyrosine and phosphothreonine residues on ERK-2 (MAPK1) to inactivate the ERK-2 kinase.	Phosphothreonine	105-121	dual specificity phosphatase 6	Homo sapiens	61-66
20594154-7	2010	The data show that glutamic acid 248, asparagine 267 and, to a lesser extent, arginine 299 are important for the interaction between the MKP3 C-terminal and the N-terminal domains.	Glutamic Acid	19-32	dual specificity phosphatase 6	Homo sapiens	137-141
20594154-7	2010	The data show that glutamic acid 248, asparagine 267 and, to a lesser extent, arginine 299 are important for the interaction between the MKP3 C-terminal and the N-terminal domains.	Asparagine	38-48	dual specificity phosphatase 6	Homo sapiens	137-141
20594154-7	2010	The data show that glutamic acid 248, asparagine 267 and, to a lesser extent, arginine 299 are important for the interaction between the MKP3 C-terminal and the N-terminal domains.	Arginine	78-86	dual specificity phosphatase 6	Homo sapiens	137-141
19563823-3	2009	In contrast, some other genes, including DUSP6, CYR61, and F3, showed sustained upregulation in senescent HDFs later after LPA treatment.	lysophosphatidic acid	123-126	dual specificity phosphatase 6	Homo sapiens	41-46
20554528-0	2010	Differential up-regulation of MAP kinase phosphatases MKP3/DUSP6 and DUSP5 by Ets2 and c-Jun converge in the control of the growth arrest versus proliferation response of MCF-7 breast cancer cells to phorbol ester.	Phorbol Esters	200-213	dual specificity phosphatase 6	Homo sapiens	54-58
20554528-0	2010	Differential up-regulation of MAP kinase phosphatases MKP3/DUSP6 and DUSP5 by Ets2 and c-Jun converge in the control of the growth arrest versus proliferation response of MCF-7 breast cancer cells to phorbol ester.	Phorbol Esters	200-213	dual specificity phosphatase 6	Homo sapiens	59-64
19476641-4	2009	RESULTS: JWH015 (a CBR2 agonist) increased MKP-1 and MKP-3 expression, which in turn reduced p-ERK1/2 in LPS-stimulated primary microglia.	JHW 015	9-15	dual specificity phosphatase 6	Homo sapiens	53-58
19476641-8	2009	However, the inhibition of both MKP-1 and MKP-3 by triptolide induced an increase in p-ERK expression and in microglial migration using LPS+JWH015-treated microglia.	triptolide	51-61	dual specificity phosphatase 6	Homo sapiens	42-47
19476641-8	2009	However, the inhibition of both MKP-1 and MKP-3 by triptolide induced an increase in p-ERK expression and in microglial migration using LPS+JWH015-treated microglia.	JHW 015	140-146	dual specificity phosphatase 6	Homo sapiens	42-47
19109160-14	2009	This synergistic effect on MUC5AC production may be due to enhanced activation of ERK through inhibition of MKP3 by poly(I:C).	poly	116-120	dual specificity phosphatase 6	Homo sapiens	108-112
19028102-0	2009	Bioactivities of simplified adociaquinone B and naphthoquinone derivatives against Cdc25B, MKP-1, and MKP-3 phosphatases.	adociaquinone B	28-43	dual specificity phosphatase 6	Homo sapiens	102-107
19028102-0	2009	Bioactivities of simplified adociaquinone B and naphthoquinone derivatives against Cdc25B, MKP-1, and MKP-3 phosphatases.	Naphthoquinones	48-62	dual specificity phosphatase 6	Homo sapiens	102-107
19106095-5	2009	We could also demonstrate that PDGF-BB stimulation induces phosphorylation of MKP3 at Ser-174 and Ser-300; phosphorylation of Ser-174 is involved in PDGF-induced MKP3 degradation, since mutation of this site stabilized MKP3.	Serine	86-89	dual specificity phosphatase 6	Homo sapiens	78-82
18314537-0	2008	Asbestos-induced MKP-3 expression augments TNF-alpha gene expression in human monocytes.	Asbestos	0-8	dual specificity phosphatase 6	Homo sapiens	17-22
18632752-4	2008	Intriguingly, the loss of MKP3 protein was associated with ubiquitination/proteosome degradation mediated by high intracellular reactive oxygen species (ROS) accumulation such as hydrogen peroxide in ovarian cancer cells.	Reactive Oxygen Species	128-151	dual specificity phosphatase 6	Homo sapiens	26-30
18632752-4	2008	Intriguingly, the loss of MKP3 protein was associated with ubiquitination/proteosome degradation mediated by high intracellular reactive oxygen species (ROS) accumulation such as hydrogen peroxide in ovarian cancer cells.	Reactive Oxygen Species	153-156	dual specificity phosphatase 6	Homo sapiens	26-30
18632752-4	2008	Intriguingly, the loss of MKP3 protein was associated with ubiquitination/proteosome degradation mediated by high intracellular reactive oxygen species (ROS) accumulation such as hydrogen peroxide in ovarian cancer cells.	Hydrogen Peroxide	179-196	dual specificity phosphatase 6	Homo sapiens	26-30
18632752-5	2008	Functionally, short hairpin RNA knock down of endogenous MKP3 resulted in increased ERK1/2 activity, cell proliferation rate, anchorage-independent growth ability and resistance to cisplatin in ovarian cancer cells.	Cisplatin	181-190	dual specificity phosphatase 6	Homo sapiens	57-61
18632752-7	2008	Furthermore, the enforced expression of MKP3 succeeded to sensitize ovarian cancer cells to cisplatin-induced apoptosis in vitro and in vivo.	Cisplatin	92-101	dual specificity phosphatase 6	Homo sapiens	40-44
18632752-8	2008	These results suggest a molecular mechanism by which the accumulation of ROS during ovarian cancer progression may cause the degradation of MKP3, which in turn leads to aberrant ERK1/2 activation and contributes to tumorigenicity and chemoresistance of human ovarian cancer cells.	Reactive Oxygen Species	73-76	dual specificity phosphatase 6	Homo sapiens	140-144
18314537-8	2008	We found that MKP-3 increased after exposure to asbestos, and its expression was regulated by p38.	Asbestos	48-56	dual specificity phosphatase 6	Homo sapiens	14-19
18314537-12	2008	Taken together, these data demonstrate that the p38 MAP kinase down-regulates ERK via activation of MKP-3 in human monocytes exposed to asbestos to enhance TNF-alpha gene expression.	Asbestos	136-144	dual specificity phosphatase 6	Homo sapiens	100-105
18223677-1	2008	MAP kinases phosphatases (MKPs) belong to the dual-specificity phosphatase family (DUSP) and dephosphorylate phosphothreonine and phosphotyrosine within MAP kinases.	Phosphothreonine	109-125	dual specificity phosphatase 6	Homo sapiens	83-87
18223677-1	2008	MAP kinases phosphatases (MKPs) belong to the dual-specificity phosphatase family (DUSP) and dephosphorylate phosphothreonine and phosphotyrosine within MAP kinases.	Phosphotyrosine	130-145	dual specificity phosphatase 6	Homo sapiens	83-87
18223677-6	2008	Mutagenesis studies identified serine 159 within DUSP6 as the target of the mTOR pathway.	Serine	31-37	dual specificity phosphatase 6	Homo sapiens	49-54
17046812-0	2006	Mapping ERK2-MKP3 binding interfaces by hydrogen/deuterium exchange mass spectrometry.	Hydrogen	40-48	dual specificity phosphatase 6	Homo sapiens	13-17
17131384-8	2007	The EGF-mediated time-dependent induction of MKP-3, MKP-1 and DUSP5 mRNA levels was U0126-sensitive at a concentration, which blocked EGF-mediated ERK1/2 phosphorylation but not ERK5 phosphorylation.	U 0126	84-89	dual specificity phosphatase 6	Homo sapiens	45-50
17131384-9	2007	Furthermore, U0126 inhibited EGF-induced MKP-3 and MKP-1 protein expression.	U 0126	13-18	dual specificity phosphatase 6	Homo sapiens	41-46
18374541-9	2008	Interestingly, we found that NS398 up-regulated the expression of mitogen-activated protein kinase phosphatase-1 (MKP-1) and MKP-3.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	29-34	dual specificity phosphatase 6	Homo sapiens	125-130
17459723-5	2007	Furthermore, we demonstrate the use of a 96-well plate format refolding assay in which the ERK-induced activity of MKP3 is simulated by 33% DMSO.	Dimethyl Sulfoxide	140-144	dual specificity phosphatase 6	Homo sapiens	115-119
17046812-0	2006	Mapping ERK2-MKP3 binding interfaces by hydrogen/deuterium exchange mass spectrometry.	Deuterium	49-58	dual specificity phosphatase 6	Homo sapiens	13-17
16698271-8	2006	NU-126 [2-((E)-2-(5-cyanobenzofuran-2-yl)vinyl)-1H-indole-6-carbonitrile] inhibited MKP-1 and VHR in vitro but was less active against human MKP-3, Cdc25B, and PTP1B.	nu-126	0-6	dual specificity phosphatase 6	Homo sapiens	141-146
16834321-1	2006	MAP kinase phosphatase 3 (MKP3) is a protein tyrosine phosphatase (PTP) for which in vivo evidence suggests that regulation can occur by oxidation and/or reduction of the active site cysteine.	Cysteine	183-191	dual specificity phosphatase 6	Homo sapiens	0-24
16834321-1	2006	MAP kinase phosphatase 3 (MKP3) is a protein tyrosine phosphatase (PTP) for which in vivo evidence suggests that regulation can occur by oxidation and/or reduction of the active site cysteine.	Cysteine	183-191	dual specificity phosphatase 6	Homo sapiens	26-30
16834321-2	2006	Using kinetics and mass spectrometry, we have probed the biochemical details of oxidation of the active site cysteine in MKP3, with particular focus on the mechanism of protection from irreversible inactivation to the sulfinic or sulfonic acid species.	Cysteine	109-117	dual specificity phosphatase 6	Homo sapiens	121-125
16834321-3	2006	Like other PTPs, MKP3 was found to be rapidly and reversibly inactivated by mild treatment with hydrogen peroxide.	Hydrogen Peroxide	96-113	dual specificity phosphatase 6	Homo sapiens	17-21
16834321-4	2006	We demonstrate that unlike the case for some PTPs, the sulfenic acid of the active site cysteine in MKP3 is not stabilized in the active site but instead is rapidly trapped in a re-reducible form.	Sulfenic Acids	55-68	dual specificity phosphatase 6	Homo sapiens	100-104
16834321-4	2006	We demonstrate that unlike the case for some PTPs, the sulfenic acid of the active site cysteine in MKP3 is not stabilized in the active site but instead is rapidly trapped in a re-reducible form.	Cysteine	88-96	dual specificity phosphatase 6	Homo sapiens	100-104
16834321-5	2006	Unlike the case for other PTPs, the sulfenic acid in MKP3 does not form a sulfenyl-amide species with its neighboring residue or a disulfide with a single proximate cysteine.	Sulfenic Acids	36-49	dual specificity phosphatase 6	Homo sapiens	53-57
16740736-4	2006	Overexpression of MKP3 rendered ER-alpha-positive breast cancer cells resistant to the growth-inhibitory effects of tamoxifen and enhanced tamoxifen agonist activity in endometrial cells.	Tamoxifen	116-125	dual specificity phosphatase 6	Homo sapiens	18-22
16740736-4	2006	Overexpression of MKP3 rendered ER-alpha-positive breast cancer cells resistant to the growth-inhibitory effects of tamoxifen and enhanced tamoxifen agonist activity in endometrial cells.	Tamoxifen	139-148	dual specificity phosphatase 6	Homo sapiens	18-22
16740736-5	2006	MKP3 overexpression was associated with lower levels of activated extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in the presence of estrogen but that estrogen deprivation and tamoxifen treatment decreased MKP3 phosphatase activity, leading to an up-regulation of pERK1/2 MAPK, phosphorylated Ser(118)-ER-alpha, and cyclin D1.	Tamoxifen	195-204	dual specificity phosphatase 6	Homo sapiens	0-4
16740736-5	2006	MKP3 overexpression was associated with lower levels of activated extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in the presence of estrogen but that estrogen deprivation and tamoxifen treatment decreased MKP3 phosphatase activity, leading to an up-regulation of pERK1/2 MAPK, phosphorylated Ser(118)-ER-alpha, and cyclin D1.	Tamoxifen	195-204	dual specificity phosphatase 6	Homo sapiens	225-229
16740736-5	2006	MKP3 overexpression was associated with lower levels of activated extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in the presence of estrogen but that estrogen deprivation and tamoxifen treatment decreased MKP3 phosphatase activity, leading to an up-regulation of pERK1/2 MAPK, phosphorylated Ser(118)-ER-alpha, and cyclin D1.	Serine	312-315	dual specificity phosphatase 6	Homo sapiens	0-4
16740736-7	2006	Accumulation of reactive oxygen species was observed with tamoxifen treatment of MKP3-overexpressing cells, and antioxidant treatment increased MKP3 phosphatase activity, thereby blocking resistance.	Reactive Oxygen Species	16-39	dual specificity phosphatase 6	Homo sapiens	81-85
16740736-7	2006	Accumulation of reactive oxygen species was observed with tamoxifen treatment of MKP3-overexpressing cells, and antioxidant treatment increased MKP3 phosphatase activity, thereby blocking resistance.	Tamoxifen	58-67	dual specificity phosphatase 6	Homo sapiens	81-85
16740736-8	2006	Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	dual specificity phosphatase 6	Homo sapiens	115-119
16740736-8	2006	Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	dual specificity phosphatase 6	Homo sapiens	176-180
16740736-8	2006	Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells.	Tamoxifen	97-106	dual specificity phosphatase 6	Homo sapiens	115-119
16740736-8	2006	Furthermore, PD98059 increased the levels of phosphorylated c-Jun NH(2)-terminal kinase (JNK) in tamoxifen-treated MKP3-overexpressing cells, suggesting an interaction between MKP3 levels, activation of ERK1/2 MAPK, and JNK signaling in human breast cancer cells.	Tamoxifen	97-106	dual specificity phosphatase 6	Homo sapiens	176-180
16740736-9	2006	MKP3 represents a novel mechanism of resistance, which may be a potential biomarker for the use of ERK1/2 and/or JNK inhibitors in combination with tamoxifen treatment.	Tamoxifen	148-157	dual specificity phosphatase 6	Homo sapiens	0-4
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	15-23	dual specificity phosphatase 6	Homo sapiens	100-105
16740736-0	2006	Elevated expression of mitogen-activated protein kinase phosphatase 3 in breast tumors: a mechanism of tamoxifen resistance.	Tamoxifen	103-112	dual specificity phosphatase 6	Homo sapiens	23-69
16740736-3	2006	Gene expression profiling was used to identify mitogen-activated protein kinase (MAPK) phosphatase 3 (MKP3) whose expression was correlated with response to the antiestrogen tamoxifen in both patients and in vitro-derived cell line models.	Tamoxifen	174-183	dual specificity phosphatase 6	Homo sapiens	102-106
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	140-148	dual specificity phosphatase 6	Homo sapiens	100-105
16012519-4	2005	The pattern of retinoid responsiveness for six of 13 target genes (RARbeta2, CYP26A1, CRBP1, RGS16, DUSP6, EGR1) correlated with phenotypic retinoid sensitivity, across a panel of retinoid-sensitive or -resistant lung and breast cancer cell lines.	Retinoids	140-148	dual specificity phosphatase 6	Homo sapiens	100-105
16012519-8	2005	Combined, rather than individual, inhibition of DUSP6 and RGS16 was required to block retinoid-induced growth inhibition in neuroblastoma cells, through phosphorylation of extracellular-signal-regulated kinase.	Retinoids	86-94	dual specificity phosphatase 6	Homo sapiens	48-53
16012519-9	2005	In conclusion, sensitivity to the retinoid anticancer signal is determined in part by the transcriptional response of key retinoid-regulated target genes, such as RARbeta2, DUSP6, and RGS16.	Retinoids	34-42	dual specificity phosphatase 6	Homo sapiens	173-178
16012519-9	2005	In conclusion, sensitivity to the retinoid anticancer signal is determined in part by the transcriptional response of key retinoid-regulated target genes, such as RARbeta2, DUSP6, and RGS16.	Retinoids	122-130	dual specificity phosphatase 6	Homo sapiens	173-178
15269220-3	2004	We have used MKP-3-green fluorescent protein fusions in conjunction with leptomycin B to show that the cytoplasmic localization of MKP-3 is mediated by a chromosome region maintenance-1 (CRM1)-dependent nuclear export pathway.	leptomycin B	73-85	dual specificity phosphatase 6	Homo sapiens	131-136
15753082-5	2005	Sanguinarine inhibited cellular MKP-1 with an IC50 of 10 microM and showed selectivity for MKP-1 over MKP-3.	sanguinarine	0-12	dual specificity phosphatase 6	Homo sapiens	102-107
15753082-6	2005	Sanguinarine also inhibited MKP-1 and the MKP-1 like phosphatase, MKP-L, in vitro with IC50 values of 17.3 and 12.5 microM, respectively, and showed 5-10-fold selectivity for MKP-3 and MKP-1 over VH-1-related phosphatase, Cdc25B2, or protein-tyrosine phosphatase 1B.	sanguinarine	0-12	dual specificity phosphatase 6	Homo sapiens	175-180
15824892-5	2005	We observed restored expression of DUSP6 after treatment with 5-azacytidine and trichostatin A, a DNA methyltransferase inhibitor and a histone deacetylase inhibitor, respectively, in cells with intrinsically very-low-level and low-level expression of DUSP6.	Azacitidine	62-75	dual specificity phosphatase 6	Homo sapiens	35-40
15824892-5	2005	We observed restored expression of DUSP6 after treatment with 5-azacytidine and trichostatin A, a DNA methyltransferase inhibitor and a histone deacetylase inhibitor, respectively, in cells with intrinsically very-low-level and low-level expression of DUSP6.	Azacitidine	62-75	dual specificity phosphatase 6	Homo sapiens	252-257
15824892-5	2005	We observed restored expression of DUSP6 after treatment with 5-azacytidine and trichostatin A, a DNA methyltransferase inhibitor and a histone deacetylase inhibitor, respectively, in cells with intrinsically very-low-level and low-level expression of DUSP6.	trichostatin A	80-94	dual specificity phosphatase 6	Homo sapiens	35-40
15824892-5	2005	We observed restored expression of DUSP6 after treatment with 5-azacytidine and trichostatin A, a DNA methyltransferase inhibitor and a histone deacetylase inhibitor, respectively, in cells with intrinsically very-low-level and low-level expression of DUSP6.	trichostatin A	80-94	dual specificity phosphatase 6	Homo sapiens	252-257
15824892-6	2005	Using a sodium-bisulfite-modification assay, we found that CpG sequences in intron 1 of DUSP6 were heavily methylated in MIA PaCa-2 and PAN07JCK, both showing the very low level of intrinsic expression of the gene.	sodium bisulfite	8-24	dual specificity phosphatase 6	Homo sapiens	88-93
15632084-0	2005	Extracellular signal-regulated kinases phosphorylate mitogen-activated protein kinase phosphatase 3/DUSP6 at serines 159 and 197, two sites critical for its proteasomal degradation.	Serine	109-116	dual specificity phosphatase 6	Homo sapiens	100-105
15632084-3	2005	Using a fibroblast model in which the expression of either MKP-3 or a more stable MKP-3-green fluorescent protein (GFP) chimera was induced by tetracycline, we found that serum induces the phosphorylation of MKP-3 and its subsequent degradation by the proteasome in a MEK1 and MEK2 (MEK1/2)-ERK1/2-dependent manner.	Tetracycline	143-155	dual specificity phosphatase 6	Homo sapiens	59-64
15632084-3	2005	Using a fibroblast model in which the expression of either MKP-3 or a more stable MKP-3-green fluorescent protein (GFP) chimera was induced by tetracycline, we found that serum induces the phosphorylation of MKP-3 and its subsequent degradation by the proteasome in a MEK1 and MEK2 (MEK1/2)-ERK1/2-dependent manner.	Tetracycline	143-155	dual specificity phosphatase 6	Homo sapiens	82-87
15632084-3	2005	Using a fibroblast model in which the expression of either MKP-3 or a more stable MKP-3-green fluorescent protein (GFP) chimera was induced by tetracycline, we found that serum induces the phosphorylation of MKP-3 and its subsequent degradation by the proteasome in a MEK1 and MEK2 (MEK1/2)-ERK1/2-dependent manner.	Tetracycline	143-155	dual specificity phosphatase 6	Homo sapiens	82-87
15632084-4	2005	In vitro phosphorylation assays using glutathione S-transferase (GST)-MKP-3 fusion proteins indicated that ERK2 could phosphorylate MKP-3 on serines 159 and 197.	Serine	141-148	dual specificity phosphatase 6	Homo sapiens	70-75
15632084-4	2005	In vitro phosphorylation assays using glutathione S-transferase (GST)-MKP-3 fusion proteins indicated that ERK2 could phosphorylate MKP-3 on serines 159 and 197.	Serine	141-148	dual specificity phosphatase 6	Homo sapiens	132-137
15632084-5	2005	Tetracycline-inducible cell clones expressing either single or double serine mutants of MKP-3 or MKP-3-GFP confirmed that these two sites are targeted by the MEK1/2-ERK1/2 module in vivo.	Tetracycline	0-12	dual specificity phosphatase 6	Homo sapiens	88-93
15632084-5	2005	Tetracycline-inducible cell clones expressing either single or double serine mutants of MKP-3 or MKP-3-GFP confirmed that these two sites are targeted by the MEK1/2-ERK1/2 module in vivo.	Tetracycline	0-12	dual specificity phosphatase 6	Homo sapiens	97-102
15632084-5	2005	Tetracycline-inducible cell clones expressing either single or double serine mutants of MKP-3 or MKP-3-GFP confirmed that these two sites are targeted by the MEK1/2-ERK1/2 module in vivo.	Serine	70-76	dual specificity phosphatase 6	Homo sapiens	88-93
15632084-5	2005	Tetracycline-inducible cell clones expressing either single or double serine mutants of MKP-3 or MKP-3-GFP confirmed that these two sites are targeted by the MEK1/2-ERK1/2 module in vivo.	Serine	70-76	dual specificity phosphatase 6	Homo sapiens	97-102
15632084-6	2005	Double serine mutants of MKP-3 or MKP-3-GFP were more efficiently protected from degradation than single mutants or wild-type MKP-3, indicating that phosphorylation of either serine by ERK1/2 enhances proteasomal degradation of MKP-3.	Serine	7-13	dual specificity phosphatase 6	Homo sapiens	25-30
15632084-6	2005	Double serine mutants of MKP-3 or MKP-3-GFP were more efficiently protected from degradation than single mutants or wild-type MKP-3, indicating that phosphorylation of either serine by ERK1/2 enhances proteasomal degradation of MKP-3.	Serine	175-181	dual specificity phosphatase 6	Homo sapiens	25-30
15632084-6	2005	Double serine mutants of MKP-3 or MKP-3-GFP were more efficiently protected from degradation than single mutants or wild-type MKP-3, indicating that phosphorylation of either serine by ERK1/2 enhances proteasomal degradation of MKP-3.	Serine	175-181	dual specificity phosphatase 6	Homo sapiens	34-39
15632084-6	2005	Double serine mutants of MKP-3 or MKP-3-GFP were more efficiently protected from degradation than single mutants or wild-type MKP-3, indicating that phosphorylation of either serine by ERK1/2 enhances proteasomal degradation of MKP-3.	Serine	175-181	dual specificity phosphatase 6	Homo sapiens	34-39
15632084-6	2005	Double serine mutants of MKP-3 or MKP-3-GFP were more efficiently protected from degradation than single mutants or wild-type MKP-3, indicating that phosphorylation of either serine by ERK1/2 enhances proteasomal degradation of MKP-3.	Serine	175-181	dual specificity phosphatase 6	Homo sapiens	34-39
15269220-4	2004	Furthermore, the nuclear translocation of MKP-3 seen in the presence of leptomycin B is mediated by an active process, indicating that MKP-3 shuttles between the nucleus and cytoplasm.	leptomycin B	72-84	dual specificity phosphatase 6	Homo sapiens	42-47
15269220-4	2004	Furthermore, the nuclear translocation of MKP-3 seen in the presence of leptomycin B is mediated by an active process, indicating that MKP-3 shuttles between the nucleus and cytoplasm.	leptomycin B	72-84	dual specificity phosphatase 6	Homo sapiens	135-140
15159408-5	2004	Palytoxin induced the loss of MKP-3 in a manner that corresponded to increased ERK phosphorylation.	palytoxin	0-9	dual specificity phosphatase 6	Homo sapiens	30-35
15159408-6	2004	Complementary studies showed that sustained expression of exogenous MKP-3 inhibited palytoxin-stimulated ERK activation.	palytoxin	84-93	dual specificity phosphatase 6	Homo sapiens	68-73
15159408-8	2004	To investigate whether expression of oncogenic Ras is key to palytoxin-stimulated ERK activation, we determined how palytoxin affected ERK and MKP-3 in MCF10A human breast epithelial cells and in H-ras MCF10A cells, which stably express activated H-Ras.	palytoxin	116-125	dual specificity phosphatase 6	Homo sapiens	143-148
15159408-11	2004	Strikingly, palytoxin stimulated ERK activity and induced a corresponding loss of MKP-3 in H-ras MCF10A cells.	palytoxin	12-21	dual specificity phosphatase 6	Homo sapiens	82-87
15159408-12	2004	These studies indicate that in initiated cells palytoxin unleashes ERK activity by down-regulating MKP-3, an ERK inhibitor, and further suggest that MKP-3 may be a vulnerable target in cells that express oncogenic Ras.	palytoxin	47-56	dual specificity phosphatase 6	Homo sapiens	99-104
15159408-12	2004	These studies indicate that in initiated cells palytoxin unleashes ERK activity by down-regulating MKP-3, an ERK inhibitor, and further suggest that MKP-3 may be a vulnerable target in cells that express oncogenic Ras.	palytoxin	47-56	dual specificity phosphatase 6	Homo sapiens	149-154
15255957-3	2004	We compared expression of Tbx3, the gene associated with the human condition ulnar-mammary syndrome, expression of the gene encoding the dual-specificity MAPK phosphatase Pyst1/MKP3, which is an early response to FGFR1 signalling (as judged by sensitivity to the SU5402 inhibitor), and expression of Lef1, encoding a transcription factor mediating Wnt signalling and the earliest gene so far known to be expressed in mammary gland development.	SU 5402	263-269	dual specificity phosphatase 6	Homo sapiens	171-176
15255957-3	2004	We compared expression of Tbx3, the gene associated with the human condition ulnar-mammary syndrome, expression of the gene encoding the dual-specificity MAPK phosphatase Pyst1/MKP3, which is an early response to FGFR1 signalling (as judged by sensitivity to the SU5402 inhibitor), and expression of Lef1, encoding a transcription factor mediating Wnt signalling and the earliest gene so far known to be expressed in mammary gland development.	SU 5402	263-269	dual specificity phosphatase 6	Homo sapiens	177-181
12840032-0	2003	Constitutive induction of p-Erk1/2 accompanied by reduced activities of protein phosphatases 1 and 2A and MKP3 due to reactive oxygen species during cellular senescence.	Reactive Oxygen Species	118-141	dual specificity phosphatase 6	Homo sapiens	106-110
15240129-4	2004	We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN, the MAP kinase phosphatase-3, MKP-3, and the protein tyrosine phosphatase, SHP2.	Indomethacin	14-26	dual specificity phosphatase 6	Homo sapiens	125-149
15240129-4	2004	We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN, the MAP kinase phosphatase-3, MKP-3, and the protein tyrosine phosphatase, SHP2.	Indomethacin	14-26	dual specificity phosphatase 6	Homo sapiens	151-156
15240129-4	2004	We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN, the MAP kinase phosphatase-3, MKP-3, and the protein tyrosine phosphatase, SHP2.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	31-37	dual specificity phosphatase 6	Homo sapiens	125-149
15240129-4	2004	We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN, the MAP kinase phosphatase-3, MKP-3, and the protein tyrosine phosphatase, SHP2.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	31-37	dual specificity phosphatase 6	Homo sapiens	151-156
15541888-14	2004	The data show an increased expression of MKP-1 and MKP-3 during hypoxia in neuronal nuclei of newborn piglets and the administration of 7-NINA, an nNOS inhibitor, prevented the hypoxia-induced increased expression of MKP-1 and MKP-3.	7-nitroindazole	136-142	dual specificity phosphatase 6	Homo sapiens	51-56
15541888-14	2004	The data show an increased expression of MKP-1 and MKP-3 during hypoxia in neuronal nuclei of newborn piglets and the administration of 7-NINA, an nNOS inhibitor, prevented the hypoxia-induced increased expression of MKP-1 and MKP-3.	7-nitroindazole	136-142	dual specificity phosphatase 6	Homo sapiens	227-232
15541888-19	2004	We conclude that hypoxia-induced decrease in MKP-1 and MKP-3 activity is not due to altered expression but due to NO-mediated modification of the cysteine residue at the active site of these dual specificity phosphatases, a mechanism of their inactivation that leads to activation of MAP kinases.	Cysteine	146-154	dual specificity phosphatase 6	Homo sapiens	55-60
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Cadmium	26-28	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Cadmium	26-28	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Glutamic Acid	47-50	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Glutamic Acid	47-50	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Tyrosine	55-58	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Tyrosine	55-58	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Arginine	64-67	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Arginine	64-67	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	73-76	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	73-76	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Tyrosine	82-85	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Tyrosine	82-85	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	91-94	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	91-94	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	91-94	dual specificity phosphatase 6	Homo sapiens	144-148
12754209-4	2003	Thus, the common docking (CD) site composed of Glu-79, Tyr-126, Arg-133, Asp-160, Tyr-314, Asp-316, and Asp-319 are important for high affinity MKP3 binding but not essential for ERK2-induced MKP3 activation.	Aspartic Acid	91-94	dual specificity phosphatase 6	Homo sapiens	192-196
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Tyrosine	34-37	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Threonine	43-46	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Leucine	52-55	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Lysine	61-64	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Arginine	70-73	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Tryptophan	79-82	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Glutamic Acid	88-91	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Arginine	97-100	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Lysine	106-109	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-5	2003	MKP3 activation requires residues Tyr-111, Thr-116, Leu-119, Lys-149, Arg-189, Trp-190, Glu-218, Arg-223, Lys-229, and His-230 in the ERK2 substrate-binding region, located distal to the common docking site.	Histidine	119-122	dual specificity phosphatase 6	Homo sapiens	0-4
12754209-8	2003	There is evidence indicating that the CD site and the substrate-binding region defined here are also utilized for MEK1 recognition, and indeed, we demonstrate that the binding of MKP3, Elk1, and MEK1 to ERK2 is mutually exclusive.	Cadmium	38-40	dual specificity phosphatase 6	Homo sapiens	179-183
12754209-10	2003	In this model, one part of the ERK2-binding proteins (e.g. the kinase interaction motif sequence) docks to the CD site located on the back side of the ERK2 catalytic pocket for high affinity association, whereas the interaction of the substrate-binding region with another structural element (e.g. the FXFP motif in MKP3 and Elk1) may not only stabilize binding but also provide contacts crucial for modulating the activity and/or specificity of ERK2 target molecules.	Cadmium	111-113	dual specificity phosphatase 6	Homo sapiens	316-320