HCSGD entry for DUSP6

1. General information

Official gene symbolDUSP6
Entrez ID1848
Gene full namedual specificity phosphatase 6
Other gene symbolsMKP3 PYST1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000188Inactivation of MAPK activityIDAbiological_process
GO:0001933Negative regulation of protein phosphorylationIEAbiological_process
GO:0002224Toll-like receptor signaling pathwayTASbiological_process
GO:0002755MyD88-dependent toll-like receptor signaling pathwayTASbiological_process
GO:0002756MyD88-independent toll-like receptor signaling pathwayTASbiological_process
GO:0004725Protein tyrosine phosphatase activityIEAmolecular_function
GO:0005654NucleoplasmTAScellular_component
GO:0005737CytoplasmIDA IEAcellular_component
GO:0005829CytosolIBAcellular_component
GO:0006470Protein dephosphorylationIEAbiological_process
GO:0008138Protein tyrosine/serine/threonine phosphatase activityIEAmolecular_function
GO:0009953Dorsal/ventral pattern formationIBAbiological_process
GO:0014070Response to organic cyclic compoundIEAbiological_process
GO:0017017MAP kinase tyrosine/serine/threonine phosphatase activityIDA IEAmolecular_function
GO:0030154Cell differentiationIEAbiological_process
GO:0034134Toll-like receptor 2 signaling pathwayTASbiological_process
GO:0034138Toll-like receptor 3 signaling pathwayTASbiological_process
GO:0034142Toll-like receptor 4 signaling pathwayTASbiological_process
GO:0034146Toll-like receptor 5 signaling pathwayTASbiological_process
GO:0034162Toll-like receptor 9 signaling pathwayTASbiological_process
GO:0034166Toll-like receptor 10 signaling pathwayTASbiological_process
GO:0035335Peptidyl-tyrosine dephosphorylationIDAbiological_process
GO:0035666TRIF-dependent toll-like receptor signaling pathwayTASbiological_process
GO:0038123Toll-like receptor TLR1:TLR2 signaling pathwayTASbiological_process
GO:0038124Toll-like receptor TLR6:TLR2 signaling pathwayTASbiological_process
GO:0040036Regulation of fibroblast growth factor receptor signaling pathwayIBAbiological_process
GO:0042493Response to drugIEAbiological_process
GO:0042663Regulation of endodermal cell fate specificationIBAbiological_process
GO:0043065Positive regulation of apoptotic processIDAbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0048011Neurotrophin TRK receptor signaling pathwayTASbiological_process
GO:0051403Stress-activated MAPK cascadeTASbiological_process
GO:0051409Response to nitrosative stressIEPbiological_process
GO:0060420Regulation of heart growthIBA IEAbiological_process
GO:0070373Negative regulation of ERK1 and ERK2 cascadeIEA IMPbiological_process
GO:0070848Response to growth factorIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00009615140.77315410890.02777526881.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up2.4968603426
GSE13712_SHEARDown-0.5770286170
GSE13712_STATICUp0.3376330927
GSE19018Down-0.5688656314
GSE19899_A1Up3.0423941226
GSE19899_A2Up2.4930531962
PubMed_21979375_A1Up2.9103251408
PubMed_21979375_A2Up2.6430937974
GSE35957Down-1.1851635503
GSE36640Up2.6841536399
GSE54402Up2.4943657518
GSE9593Up0.3570168736
GSE43922Up1.5499675903
GSE24585Down-0.0937627673
GSE37065Up0.8222905682
GSE28863_A1Up0.0477614397
GSE28863_A2Down-0.1596370301
GSE28863_A3Down-0.3407997830
GSE28863_A4Up0.1637629955
GSE48662Up0.6346004914

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL1672295CHEMBL12503818Q16828
CHEMBL1672294CHEMBL12503818Q16828
CHEMBL1672293CHEMBL12503818Q16828
CHEMBL1672291CHEMBL12503818Q16828
CHEMBL1241589CHEMBL12503818Q16828
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  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-181a-5pMIMAT0000256MIRT006481Luciferase reporter assay//Western blotFunctional MTI17382377
hsa-miR-335-5pMIMAT0000765MIRT018633MicroarrayFunctional MTI (Weak)18185580
hsa-miR-375MIMAT0000728MIRT020032MicroarrayFunctional MTI (Weak)20215506
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 6 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27354409We have previously shown a decline in miR-181a, which regulates CD4+ T cell responses via DUSP6 overexpression, in individuals with hepatitis C virus (HCV) infection
25477247Hepatitis C virus-induced reduction in miR-181a impairs CD4(+) T-cell responses through overexpression of DUSP6
25477247Here, we demonstrate that hepatitis C virus (HCV)-mediated decline of miR-181a expression impairs CD4(+) T-cell responses through overexpression of dual specific phosphatase 6 (DUSP6)
25477247Specifically, a significant decline of miR-181a expression along with overexpression of DUSP6 was observed in CD4(+) T cells from chronically HCV-infected individuals compared to healthy subjects, and the levels of miR-181a loss were found to be negatively associated with the levels of DUSP6 overexpression in these cells
25477247CONCLUSION: Since a decline of miR-181a concomitant with DUSP6 overexpression is the signature marker for age-associated T-cell senescence, these findings provide novel mechanistic insights into HCV-mediated premature T-cell aging through miR-181a-regulated DUSP6 signaling and reveal new targets for therapeutic rejuvenation of impaired T-cell responses during chronic viral infection
25414256Further analysis revealed that senescent cells expressed a significantly higher level of mitogen-activated protein phosphatase 3 (MKP-3, a cytosolic ERK1/2-targeted phosphatase), which was suppressed by blocking the transcriptional activity of the tumor suppressor p53 with pifithrin-alpha
25414256Inhibition of MKP-3 activity with a specific inhibitor or siRNA enhanced basal ERK1/2 phosphorylation and promoted cell proliferation
25414256These results therefore indicate that p53-mediated up-regulation of MKP-3 contributes to the establishment of the senescent cellular phenotype through dephosphorylating ERK1/2
19563823In contrast, some other genes, including DUSP6, CYR61, and F3, showed sustained upregulation in senescent HDFs later after LPA treatment
17658517Cells were induced to senescence by inhibition of phosphatase activity (VHR, MKP3, or PP2A) without additional cellular stress
12840032Constitutive 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
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