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FLASH GENE
Symbol DUSP4 contributors: mct/npt/pgu - updated : 31-08-2018
HGNC name dual specificity phosphatase 4
HGNC id 3070
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • two N terminal CH2 domains
  • an extended active site sequence motif conserved in dual specificity phosphatases
    • HOMOLOGY
    Homologene
    FAMILY
  • protein-tyrosine phosphatase family
  • non-receptor class dual specificity subfamily
    • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    intracellular,nucleus,nucleoplasm
    text
  • nuclear located enzyme
    • basic FUNCTION
  • involved, with DUSP2 in stimulus-specific, and phosphatase-specific mechanism of MAPK1 regulation in the nucleus
  • part of a heterogeneous group of protein phosphatases that can dephosphorylate both phosphotyrosine and phosphoserine/phosphothreonine residues within the one substrate
  • involved in negative feedback control of EGFR signaling
  • having functions to inactivate the ERK and JNK MAP kinase signalling pathways
  • critical non-redundant role in regulating cell cycle progression and apoptosis
  • required for cardiac fibroblast and macrophage proliferation
  • essential role in protecting cellular integrity
  • plays potentially opposing roles in different types of cancer depending on which kinase, ERK or JNK, is being preferentially regulated in that cell type
  • MAP kinase-induced DUSP member that is dynamically expressed during thymocyte differentiation
  • DUSP4 causes cardiac dysfunction and may contribute to the development of LMNA cardiomyopathy
  • attenuates ERK signaling and reduces cell viability, suggesting that the novel crosstalk between NFKB1 and MAPK pathways contributes to cell survival
  • DUSP4 is crucial for neuronal differentiation and functions in the neurogenesis of embryonic stem cells (ESCs)
  • regulates neuronal differentiation and calcium homeostasis by modulating ERK1/2 phosphorylation
  • is important for helper T cell development, and there is a DUSP4-mediated regulation of STAT5B protein stability
  • is a critical regulator of the growth and invasion of triple-negative breast cancer cells
  • is crucial in regulating corticosteroid sensitivity
  • is a key contributor to the pathogenesis of LMNA cardiomyopathy
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling signal transduction
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • bound ERK and to a lesser extent JNK
  • DUSP4 suppresses CD4(+) T-cell proliferation through novel regulations in STAT5B phosphorylation and IL2 signaling
  • TNF caused a significant suppression of a dual specificity phosphatase, DUSP4, that regulates ERK1/2 activation
  • DUSP4 regulates STAT5B protein stability and helper T cell polarization
    • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in senescent fibroblasts, compared to their young counterparts
    tumoral somatic mutation     gain of function
    activating KRAS mutations is significantly correlated to an upregulation of 13 genes among them DUSP4, a MAP-kinase phosphatase, and SMYD3 in colorectal cancer
    tumoral     --low  
    through activation of the MAPK signaling pathway is responsible for progression of Colorectal cancer
    tumoral   deletion    
    in approximately 50 p100 of breast cancers
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
  • low DUSP4 expression levels predict recurrence and mortality in Triple-negative breast cancer (TNBC) patients independently from known clinical and molecular predictors
    • Therapy target
    SystemTypeDisorderPubmed
    respiratorylung 
    might be a novel therapeutic target in severe asthma
    ANIMAL & CELL MODELS