HCSGD entry for DUSP4


1. General information

Official gene symbolDUSP4
Entrez ID1846
Gene full namedual specificity phosphatase 4
Other gene symbolsHVH2 MKP-2 MKP2 TYP
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000165MAPK cascadeTASbiological_process
GO:0000188Inactivation of MAPK activityIBAbiological_process
GO:0001706Endoderm formationIBAbiological_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:0005634NucleusTAScellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0006470Protein dephosphorylationIBAbiological_process
GO:0008330Protein tyrosine/threonine phosphatase activityTASmolecular_function
GO:0017017MAP kinase tyrosine/serine/threonine phosphatase activityIBAmolecular_function
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: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:0045087Innate immune responseTASbiological_process
GO:0048011Neurotrophin TRK receptor signaling pathwayTASbiological_process
GO:0051403Stress-activated MAPK cascadeTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00004535540.63638866300.01882031251.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up1.3228329116
GSE13712_SHEARUp0.0351945007
GSE13712_STATICDown-0.0889992691
GSE19018Up0.0625949207
GSE19899_A1Up4.1038552910
GSE19899_A2Up7.3845250604
PubMed_21979375_A1Up6.2604311793
PubMed_21979375_A2Up7.4124918320
GSE35957Down-0.5753051462
GSE36640Up1.5482950918
GSE54402Up1.1386781319
GSE9593Up0.7112472469
GSE43922Up2.3835914277
GSE24585Down-0.3754252920
GSE37065Up0.5885240689
GSE28863_A1Down-0.4031863744
GSE28863_A2Down-0.1444599850
GSE28863_A3Up0.3033216609
GSE28863_A4Down-0.2170043702
GSE48662Up0.2591451304

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase
No target information from mirTarBase
    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25733583Intrinsic T-cell defects were caused by increased expression of dual-specific phosphatase 4 (DUSP4)
25733583Normalization of DUSP4 expression using a specific siRNA improved CD4(+) T-cell activity in ICL, as this restored TCR-induced extracellular signal-regulated kinase activation and increased the expression of the costimulatory molecules CD27 and CD40L
25733583Conversely, repeated TCR stimulation led to defective signaling and DUSP4 overexpression in control CD4(+) T cells
25733583This was associated with gradual acquisition of a memory phenotype and was curtailed by DUSP4 silencing
17145763This impairment coincides with increased activity of the nuclear ERK phosphatase MKP2
17145763Ectopic expression of MKP2 results in premature senescence
17145763In contrast, knock-down of MKP2 expression, through transduction of MKP2 sequence-specific short hairpin RNA, or expression of the phosphatase resistant ERK2(D319N) mutant, abrogates the effects of increased endogenous MKP2 levels and senescence is postponed
14567979Metabolic stabilization of MAP kinase phosphatase-2 in senescence of human fibroblasts
14567979Our results indicate that the activity and abundance of MKP-2 is increased in senescent fibroblasts, compared to their young counterparts
14567979Further analysis indicates that it is MKP-2 protein, but not MKP-2 mRNA level, that is increased in senescent cells
14567979This increase is the result of the increased stability of MKP-2 protein against proteolytic degradation
14567979Taken together, these data indicate that the increased level and activity of MKP-2 in senescent WI-38 cells are the consequence of impaired proteosomal degradation, and this increase is likely to play a significant role in the decreased levels of p-ERK in the nucleus of senescent cells
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