Affinage

DUSP10

Dual specificity protein phosphatase 10 · UniProt Q9Y6W6

Length
482 aa
Mass
52.6 kDa
Annotated
2026-06-09
57 papers in source corpus 27 papers cited in narrative 28 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DUSP10 (MKP-5) is a dual-specificity MAP kinase phosphatase that selectively binds and inactivates p38 MAPK and JNK/SAPK, with p38 as the preferred substrate and minimal activity toward ERK (PMID:10391943, PMID:10597297). Substrate selectivity is structurally encoded: its MAPK-binding domain presents an alpha-helical cluster of positively charged residues distinct from MKP3 (PMID:17400920), and it engages the p38α docking site through a non-canonical bipartite helical mode conserved across the cytoplasmic p38/JNK-specific MKP subgroup (PMID:22375048). The catalytic domain harbors an allosteric pocket whose integrity depends on residue Y435; this residue couples pocket conformation to active-site organization and is itself required for p38 and JNK binding, and a small molecule occupying this pocket collapses the active site and recapitulates DUSP10 loss (PMID:32843541, PMID:36116232, PMID:40745179). Through suppression of p38 and JNK, DUSP10 acts as a brake on inflammatory and stress signaling in multiple tissues: it restrains neutrophil p38→p47phox-driven superoxide production (PMID:19696743), limits IL-33→p38→GATA3-dependent IL-5 production in pathogenic Th2 cells (PMID:30315197), and negatively regulates muscle satellite cell proliferation (via JNK) and differentiation (via p38) (PMID:23543058). DUSP10 promotes tissue fibrosis by supporting TGF-β/SMAD signaling through a JNK-dependent mechanism, and its loss protects against pulmonary and hepatic fibrosis (PMID:31483681, PMID:39609656). DUSP10 protein abundance is set post-translationally by opposing modifications: mTORC2 binds and phosphorylates it on Ser224/Ser230 to block turnover (PMID:25568665), whereas the E3 ligase TRIM7 ubiquitinates it to drive proteasomal degradation, relieving inhibition of IKKβ-NF-κB and JNK/p38 in fatty liver disease (PMID:41290618). Its expression is further constrained by epigenetic silencing (STAT3/SETD8) and multiple miRNAs and induced by HMW-HA/CD44 signaling (PMID:33232789, PMID:40002789).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1999 High

    Established DUSP10's core biochemical identity: that it is a phosphatase with defined MAPK substrate selectivity, distinguishing it from the broad family of phosphatases.

    Evidence In vitro phosphatase and binding assays plus immunoprecipitation with catalytically inactive mutant in mammalian cells

    PMID:10391943 PMID:10597297

    Open questions at the time
    • Structural basis of p38/JNK vs ERK selectivity not resolved
    • Physiological substrates in vivo not yet addressed
  2. 2007 High

    Resolved why DUSP10's substrate preference differs from related MKPs by showing its MAPK-binding domain uses an alpha-helical positive-charge cluster rather than the loop/beta-strand arrangement of MKP3.

    Evidence X-ray crystallography of isolated binding and catalytic domains of human MKP5

    PMID:17400920

    Open questions at the time
    • Domain structures solved in isolation, not in complex with a MAPK
    • Allosteric regulation of the catalytic domain not described
  3. 2011 High

    Defined the docking mechanism by capturing how the binding domain engages p38α, revealing a bipartite helical mode distinct from the classical linear docking motif and conserved across the p38/JNK-specific MKP subgroup.

    Evidence 2.7 Å co-crystal structure of p38α with the MKP5 KBD

    PMID:22375048

    Open questions at the time
    • Does not address how docking couples to catalytic turnover
    • JNK docking not directly visualized
  4. 2009 High

    Provided the first non-redundant in vivo function, showing DUSP10 specifically restrains a p38→p47phox superoxide axis in neutrophils that MKP1 does not cover.

    Evidence Mkp5-/- vs Mkp1-/- mice, neutrophil adoptive transfer, p38 inhibitor, p47phox phosphorylation and gene deletion

    PMID:19696743

    Open questions at the time
    • Mechanism of DUSP10 recruitment to neutrophil signaling not defined
    • Whether JNK contributes was not dissected
  5. 2013 High

    Showed DUSP10 partitions its two substrates to distinct cellular outputs, using JNK to gate satellite cell proliferation and p38 to gate differentiation.

    Evidence Mkp5-/- and mdx/Mkp5-/- mice, primary satellite cell assays, MAPK signaling analysis

    PMID:23543058

    Open questions at the time
    • How DUSP10 selects JNK vs p38 in a given context unresolved
    • No structural correlate of context-specific substrate choice
  6. 2014 Medium

    Identified a post-translational stabilization mechanism, placing DUSP10 abundance under mTORC2 control via Ser224/Ser230 phosphorylation.

    Evidence Co-IP, site-directed mutagenesis, phospho-mutant overexpression, xenografts in GBM cells

    PMID:25568665

    Open questions at the time
    • Single lab; kinase-substrate relationship not validated in vitro
    • Degradation machinery counteracting stabilization not identified here
  7. 2015 Medium

    Extended DUSP10's tumor-suppressive role to the intestine and linked it to ERK/KLF5, while parallel work placed it in oncogenic regulatory circuits (AGR2→DUSP10→p38→p53).

    Evidence Dusp10-/- mice in AOM/DSS model; gain/loss-of-function with phospho-readouts in cancer cell lines

    PMID:25772234 PMID:26733232

    Open questions at the time
    • ERK regulation by DUSP10 contrasts with its weak in vitro ERK activity and is not biochemically reconciled
    • Tissue-context determinants of tumor-suppressive vs oncogenic behavior unclear
  8. 2017 Medium

    Defined upstream transcriptional and signaling inputs (TP53INP1/p73 promoter regulation; HO-1/CO/cGMP induction) and added anti-apoptotic/anti-oxidant outputs in muscle, broadening the regulatory network around DUSP10.

    Evidence Cardiotoxin injury KO mice (STAT3/Bcl-2/catalase); HCC promoter analysis; endothelial siRNA and pharmacological pathway dissection

    PMID:28674078 PMID:29047406 PMID:29165873

    Open questions at the time
    • Direct binding of regulators to DUSP10 promoter not always demonstrated
    • Single-lab pathway placements
  9. 2019 High

    Consolidated DUSP10 as a tissue-protective brake on inflammation and fibrosis (Th2 IL-5 suppression, bronchial cytokine control, TGF-β/Smad coupling in lung fibroblasts) and identified a nuclear DUSP10–YAP1 interaction in colorectal cancer.

    Evidence Dusp10-/- mice and overexpression in Th2 cells; siRNA in bronchial epithelium; bleomycin fibrosis KO with Smad readouts; reciprocal Co-IP with YAP1 S397 mutant

    PMID:30315197 PMID:30333178 PMID:31483681 PMID:31717606

    Open questions at the time
    • Whether DUSP10 dephosphorylates YAP1 directly is not established
    • Mechanism coupling p38/JNK suppression to TGF-β enhancement not fully defined
  10. 2020 High

    Discovered an allosteric pocket distinct from the active site whose inhibitor occupancy collapses catalysis, giving both a druggable mechanism and a tool to recapitulate DUSP10 deficiency.

    Evidence MKP5–inhibitor co-crystal structure, phosphopeptide screen, p38/JNK activation and TGF-β1/Smad2 assays

    PMID:32843541

    Open questions at the time
    • Endogenous ligand for the allosteric pocket, if any, unknown
    • Selectivity against other MKPs not fully addressed
  11. 2022 High

    Mapped the chemical determinants of allosteric inhibition to a π-π interaction with Tyr435, pinpointing a single residue as the structural hinge of the pocket.

    Evidence Six MKP5–inhibitor crystal structures with structure-activity relationship analysis

    PMID:36116232

    Open questions at the time
    • Functional requirement of Y435 for catalysis not yet tested at this stage
    • Inhibitor in vivo efficacy not addressed
  12. 2025 High

    Unified the allosteric and catalytic story by showing Y435 maintains pocket integrity, propagates conformational changes to active-site residues, and is itself required for p38 and JNK binding and dephosphorylation.

    Evidence X-ray crystallography, NMR, molecular dynamics, and mutagenesis

    PMID:40745179

    Open questions at the time
    • How physiological inputs exploit this allosteric axis is unknown
    • Whether substrate-binding defect of Y435 mutants is independent of catalytic collapse not fully separated
  13. 2025 High

    Identified TRIM7 as the E3 ligase driving DUSP10 ubiquitination and degradation, providing the destabilizing counterpart to mTORC2 stabilization and linking DUSP10 turnover to NF-κB/MAPK hyperactivation in NAFLD.

    Evidence Co-IP, ubiquitination assay, proteasome inhibition, hepatic TRIM7 KO with DUSP10-silencing epistasis in mouse NAFLD

    PMID:41290618

    Open questions at the time
    • Ubiquitin linkage type and target residues on DUSP10 not specified
    • Coordination with mTORC2 phosphorylation not examined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DUSP10 reconciles its biochemically defined p38/JNK selectivity with reported ERK-dependent phenotypes, and how its multi-tissue context determines tumor-suppressive versus oncogenic or fibrogenic output, remains unresolved.
  • No biochemical basis for ERK regulation despite weak in vitro ERK activity
  • Context determinants of opposing physiological roles unknown
  • Direct vs indirect nature of the YAP1 interaction unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0098772 molecular function regulator activity 3 GO:0016787 hydrolase activity 2
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-392499 Metabolism of proteins 2
Partners
MAPK14MAPK8MTORTRIM7YAP1

Evidence

Reading pass · 28 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 MKP-5 (DUSP10) is a dual-specificity phosphatase that binds to p38 and SAPK/JNK but not MAPK/ERK, and selectively inactivates p38 and SAPK/JNK (with p38 as preferred substrate), while being present evenly in both cytoplasm and nucleus. Binding assays, in vitro phosphatase activity assays, subcellular fractionation/immunofluorescence The Journal of biological chemistry High 10391943 10597297
1999 MKP5 substrate selectivity (p38 ≈ JNK/SAPK >> ERK) is determined at least in part at the level of substrate binding, as demonstrated by immunoprecipitation of endogenous MAPKs with catalytically inactive MKP5. Immunoprecipitation using catalytically inactive MKP5 mutant expressed in mammalian cells Oncogene Medium 10597297
2007 Crystal structures of the MAP kinase binding domain (BD) and catalytic domain (CD) of human MKP5 were solved at up to 2.2 Å resolution. The BD of MKP5 differs dramatically from MKP3: the cluster of positively charged residues critical for MAPK binding is alpha-helical in MKP5 (vs. loop/beta-strand in MKP3), located 25 Å apart, consistent with distinct substrate preferences. The CD is in an active conformation. X-ray crystallography Protein science : a publication of the Protein Society High 17400920
2011 Crystal structure of p38α in complex with the MAPK binding domain (KBD) of MKP5 at 2.7 Å resolution revealed a bipartite binding mode in which two distinct helical regions of KBD engage the p38α docking site (on the back of the active site), distinct from the classical linear docking motif. The KBD of MKP7 closely resembles MKP5 KBD, suggesting this mechanism is conserved in the cytoplasmic p38/JNK-specific MKP subgroup. X-ray crystallography (2.7 Å resolution crystal structure of p38α–MKP5 KBD complex) Science signaling High 22375048
2009 MKP5 has a non-redundant role in restraining p38 MAPK-mediated neutrophil superoxide production: Mkp5-/- (but not Mkp1-/-) mice showed augmented p38 MAPK activation and increased superoxide generation in neutrophils; p38 MAPK phosphorylated p47phox, and p47phox gene deletion ablated LPS-induced vascular injury in Mkp5-/- mice. Genetic knockout mouse model, neutrophil depletion, adoptive transfer, p38 MAPK inhibitor (SB203580), p47phox phosphorylation assay, in vitro kinase assay The EMBO journal High 19696743
2013 MKP-5 (DUSP10) negatively regulates muscle stem cell function by controlling JNK (to coordinate proliferation) and p38 MAPK (to control differentiation); genetic loss of Mkp5 improved regenerative myogenesis and attenuated dystrophic muscle phenotype in mdx mice. Genetic knockout mouse model (Mkp5-/- and mdx/Mkp5-/- double-knockout), primary satellite cell assays, MAPK signaling analysis The Journal of clinical investigation High 23543058
2014 mTORC2 binds DUSP10 and phosphorylates it on serine residues 224 and 230, blocking DUSP10 turnover (stabilizing it), resulting in inactivation of p38 MAPK signaling. Nonphosphorylatable or phosphomimetic DUSP10 mutants confer differential mTOR kinase inhibitor responses in GBM cells. Co-immunoprecipitation, site-directed mutagenesis, ectopic overexpression of DUSP10 mutants, in vitro and xenograft cellular assays Genes & cancer Medium 25568665
2015 DUSP10 knockout mice exhibited increased intestinal epithelial cell (IEC) proliferation and migration associated with increased ERK1/2 activation and KLF5 expression, and developed more colon tumors in the AOM/DSS model, identifying DUSP10 as a negative regulator of IEC growth and a colorectal cancer suppressor. Genetic knockout mouse model, AOM/DSS colorectal cancer model, MAPK phosphorylation analysis, cell proliferation and migration assays Oncogene Medium 25772234
2015 AGR2 oncoprotein upregulates DUSP10, which subsequently inhibits p38 MAPK and prevents p53 activation by phosphorylation, defining a novel AGR2→DUSP10→p38→p53 regulatory axis in human cancer cells. Gene expression manipulation, western blot for p38 MAPK and p53 phosphorylation, pathway analysis in breast cancer cells Molecular oncology Medium 26733232
2016 High molecular weight hyaluronic acid (HA) induces DUSP10/MKP5 expression via CD44 binding, which inhibits TNF-α-induced p38 MAPK and JNK phosphorylation and AP-1 transcriptional activity, thereby suppressing MMP13 expression in chondrocytes. CD44 function-blocking antibody, siRNA knockdown, reporter assay, western blotting, immunofluorescence in human chondrocytic C28/I2 cells Journal of orthopaedic research Medium 27101204
2017 Loss of MKP-5 in skeletal muscle during regeneration activates STAT3/Bcl-2 anti-apoptotic signaling, increases catalase expression improving anti-oxidant capacity, and reduces mitochondrial apoptotic pathway activation, promoting myofiber survival. Genetic knockout mice, cardiotoxin injury model, TUNEL assay, western blot for STAT3, Bcl-2, and apoptosis markers Skeletal muscle Medium 29047406
2017 TP53INP1 downregulation promotes HCC metastasis via DUSP10 phosphatase-mediated activation of the ERK pathway; the DUSP10 promoter contains p73 binding sites directly implicated in modulation by TP53INP1. Mechanistic investigations in HCC cell lines, promoter analysis, ERK pathway activation assays Cancer research Medium 28674078
2017 Andrographolide inhibits hypoxia-induced HIF-1α and ET-1 expression through a HO-1/CO/cGMP/MKP-5 pathway: andrographolide induces HO-1 and MKP-5 expression; CO and cGMP increase MKP-5 expression; MKP-5 silencing abrogates andrographolide's suppression of p38 MAPK activation and HIF-1α expression. siRNA knockdown, pharmacological inhibitors, HO-1 inhibitor, guanylate cyclase inhibitor, western blotting in EA.hy926 endothelial cells Environmental toxicology Medium 29165873
2018 DUSP10 is expressed in ST2hi pathogenic Th2 cells but not ILC2; DUSP10 inhibits IL-33-induced cytokine production in Th2 cells by dephosphorylating and inactivating p38 MAPK, resulting in reduced GATA3 activity. Dusp10 deletion renders ST2hi Th2 cells capable of producing IL-5 upon IL-33 stimulation. Genetic knockout mice, DUSP10 overexpression in Th2 cells, p38 MAPK phosphorylation assays, GATA3 activity assays, cytokine production measurements Nature communications High 30315197
2019 MKP-5-deficient mice are protected from bleomycin-induced pulmonary fibrosis; MKP-5-deficient lung fibroblasts show enhanced p38 MAPK activity, impaired Smad3 phosphorylation, increased Smad7 levels, and decreased fibrogenic gene expression, coupling MKP-5 to the TGF-β1 signaling machinery. Genetic knockout mice, bleomycin fibrosis model, fibroblast cultures, western blot for Smad3/Smad7/p38, hydroxyproline assay, fibrogenic gene expression American journal of physiology. Lung cellular and molecular physiology Medium 31483681
2019 DUSP10 negatively regulates inflammatory cytokine production in bronchial epithelial cells in response to IL-1β stimulation (alone and in combination with rhinovirus), without affecting rhinovirus replication, as demonstrated by siRNA-mediated knockdown. siRNA knockdown, rhinovirus infection model, cytokine production assays in primary bronchial epithelial cells Journal of virology Medium 30333178
2019 DUSP10 co-immunoprecipitates with YAP1, and their interaction is dependent on YAP1 Ser397. DUSP10 nuclear localization increases at high cell density and correlates with YAP1 activity, suggesting DUSP10 acts as a regulator of YAP1 in colorectal cancer. Co-immunoprecipitation, DUSP10 overexpression/silencing, xenograft mouse model, Drosophila transgenic model, nuclear localization imaging Cancers Medium 31717606
2020 An allosteric binding pocket on MKP5 (distinct from the active site) was identified; a small-molecule inhibitor binding to this pocket collapses the MKP5 active site and limits MAPK binding. Crystal structure of MKP5 in complex with the inhibitor was solved. The inhibitor recapitulates MKP5 deficiency (activating p38 MAPK and JNK) and blocks TGF-β1-mediated Smad2 phosphorylation in muscle. X-ray crystallography (MKP5–inhibitor complex), phosphopeptide-based small-molecule screen, p38 MAPK/JNK activation assays, TGF-β1/Smad2 signaling assay Science signaling High 32843541
2020 SETD8 interacts with STAT3 and recruits SETD8 to the DUSP10 promoter region, leading to epigenetic silencing of DUSP10 expression via H4K20 methylation, resulting in constitutive ERK1/2 activation in pancreatic cancer. RNA sequencing, dual-luciferase assay, ChIP assay, mass spectrometry, SETD8 gain/loss-of-function, xenograft mouse model Cancer letters Medium 33232789
2021 Bone marrow macrophage-derived exosomal miR-143-5p targets the 3'UTR of MKP5/DUSP10 mRNA (validated by dual-luciferase reporter assay), reducing MKP5 protein levels in hepatocytes and inducing insulin resistance (decreased AKT and GSK phosphorylation); MKP5 overexpression rescues miR-143-5p-induced insulin resistance. Dual-luciferase reporter assay, western blot, miR-143-5p mimic transfection, MKP5 overexpression rescue experiment in Hep1-6 cells Cell proliferation Medium 34647385
2022 Six X-ray crystal structures of MKP5 in complex with allosteric inhibitor derivatives were solved, establishing that a parallel-displaced π-π interaction between the inhibitor three-ring core and Tyr435 is critical for modulating inhibitor potency, and that modifications to the C-9 position are essential for proper positioning. X-ray crystallography (six enzyme-inhibitor crystal structures), structure-activity relationship analysis European journal of medicinal chemistry High 36116232
2025 Residue Y435 in MKP5 is required to maintain the structural integrity of the allosteric pocket; changes in this pocket propagate conformational flexibility to reorganize catalytically crucial residues in the active site. Y435 is also required for interaction with p38 MAPK and JNK, promoting their dephosphorylation. X-ray crystallography, NMR spectroscopy, molecular dynamics simulations, mutagenesis Nature communications High 40745179
2025 E3 ligase TRIM7 interacts with DUSP10, catalyzes its ubiquitination and proteasomal degradation, leading to hyperactivation of IKKβ-NF-κB and JNK/p38 MAPK signaling pathways in the context of NAFLD. DUSP10 silencing abrogates the protective effects of TRIM7 deficiency. Co-immunoprecipitation, ubiquitination assay, proteasome inhibitor treatment, hepatic-specific TRIM7 KO, DUSP10 silencing, gain/loss-of-function in mouse NAFLD models Nature communications High 41290618
2011 ASC suppresses DUSP10/MKP5 expression in pathogen-infected macrophages (independent of caspase-1 and NLRP3), and ASC-dependent suppression of DUSP10 leads to increased MAPK (ERK) phosphorylation; MAPK activation by pathogen was abrogated in Asc-/- but not Nlrp3-/-, Nlrc4-/-, or Casp1-/- macrophages. shRNA knockdown, microarray, genetic KO macrophages (Asc-/-, Nlrp3-/-, Nlrc4-/-, Casp1-/-), TLR agonist treatment, MAPK phosphorylation assay The Journal of biological chemistry Medium 21487011
2012 MKP5 deficiency blocks ox-LDL uptake and foam cell formation in macrophages by reducing ox-LDL-induced NF-κB activation; MKP5 deficiency also inhibits TNF-α production and enhances TGF-β1 levels in ox-LDL-stimulated macrophages. Genetic knockout macrophages, foam cell formation assay, NF-κB activation assay (p65 RNAi), cytokine ELISA Cellular signalling Medium 22683306
2024 MKP-5-deficient fibroblasts are impaired in TGF-β-stimulated SMAD2 phosphorylation at canonical and non-canonical sites, nuclear translocation, and fibrogenic gene transcriptional activation; pharmacological inhibition of MKP5 blocks TGF-β signaling; this regulation occurs through a JNK-dependent pathway, as identified by RNA sequencing and transcriptomic analysis. Genetic KO fibroblasts, pharmacological MKP5 inhibitor, RNA sequencing, SMAD2 phosphorylation/nuclear translocation assays bioRxivpreprint Medium
2025 MKP5 inhibits hepatic stellate cell activation and hepatocyte apoptosis through regulation of the IRE1/XBP1 ER stress pathway; MKP5 knockout mice exhibited more pronounced hepatic fibrosis, and RNA-seq confirmed activation of endoplasmic reticulum protein processing pathway in MKP5-deficient fibrotic liver. Genetic knockout mice, CCl4 fibrosis model, RNA-seq, IRE1/XBP1 pathway analysis, HSC activation assays Journal of nanobiotechnology Medium 39609656
2025 HMW-HA binding to CD44 activates PI3K/Akt signaling and RhoA-associated protein kinase (ROK) signaling to induce DUSP10/MKP5 expression in chondrocytes; miR-92a, miR-181a, and miR-181d negatively regulate DUSP10/MKP5 expression and are suppressed by HMW-HA. PI3K/Akt inhibitors, miRNA mimic/inhibitor transfection (gain/loss-of-function), western blot for Akt phosphorylation, qRT-PCR in C28/I2 chondrocytes Biomedicines Medium 40002789

Source papers

Stage 0 corpus · 57 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Molecular cloning and characterization of a novel dual specificity phosphatase, MKP-5. The Journal of biological chemistry 200 10391943
1999 MKP5, a new member of the MAP kinase phosphatase family, which selectively dephosphorylates stress-activated kinases. Oncogene 127 10597297
2011 The NLR adaptor ASC/PYCARD regulates DUSP10, mitogen-activated protein kinase (MAPK), and chemokine induction independent of the inflammasome. The Journal of biological chemistry 64 21487011
2019 The Dual-Specificity Phosphatase 10 (DUSP10): Its Role in Cancer, Inflammation, and Immunity. International journal of molecular sciences 60 30939861
2009 A non-redundant role for MKP5 in limiting ROS production and preventing LPS-induced vascular injury. The EMBO journal 53 19696743
2013 Improved regenerative myogenesis and muscular dystrophy in mice lacking Mkp5. The Journal of clinical investigation 49 23543058
2015 AGR2 oncoprotein inhibits p38 MAPK and p53 activation through a DUSP10-mediated regulatory pathway. Molecular oncology 47 26733232
2011 A distinct interaction mode revealed by the crystal structure of the kinase p38α with the MAPK binding domain of the phosphatase MKP5. Science signaling 46 22375048
2017 TP53INP1 Downregulation Activates a p73-Dependent DUSP10/ERK Signaling Pathway to Promote Metastasis of Hepatocellular Carcinoma. Cancer research 42 28674078
2018 DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells. Nature communications 40 30315197
2013 miR-92a/DUSP10/JNK signalling axis promotes human pancreatic cancer cells proliferation. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 38 24332650
2019 p38 MAPK activation through B7-H3-mediated DUSP10 repression promotes chemoresistance. Scientific reports 37 30967582
2015 DUSP10 regulates intestinal epithelial cell growth and colorectal tumorigenesis. Oncogene 34 25772234
2019 Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis. American journal of physiology. Lung cellular and molecular physiology 31 31483681
2021 Bone marrow macrophage-derived exosomal miR-143-5p contributes to insulin resistance in hepatocytes by repressing MKP5. Cell proliferation 28 34647385
2007 Crystal structure of the MAP kinase binding domain and the catalytic domain of human MKP5. Protein science : a publication of the Protein Society 27 17400920
2020 SETD8 potentiates constitutive ERK1/2 activation via epigenetically silencing DUSP10 expression in pancreatic cancer. Cancer letters 26 33232789
2016 High molecular weight hyaluronic acid regulates MMP13 expression in chondrocytes via DUSP10/MKP5. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 26 27101204
2019 DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling. Journal of virology 21 30333178
2014 mTORC2 modulates feedback regulation of p38 MAPK activity via DUSP10/MKP5 to confer differential responses to PP242 in glioblastoma. Genes & cancer 21 25568665
2020 MKP-5 Relieves Lipotoxicity-Induced Islet β-Cell Dysfunction and Apoptosis via Regulation of Autophagy. International journal of molecular sciences 20 32998359
2019 The protective role of the MKP-5-JNK/P38 pathway in glucolipotoxicity-induced islet β-cell dysfunction and apoptosis. Experimental cell research 19 31202710
2022 MiRNA-363-3p/DUSP10/JNK axis mediates chemoresistance by enhancing DNA damage repair in diffuse large B-cell lymphoma. Leukemia 18 35488020
2020 An allosteric site on MKP5 reveals a strategy for small-molecule inhibition. Science signaling 18 32843541
2017 Loss of MKP-5 promotes myofiber survival by activating STAT3/Bcl-2 signaling during regenerative myogenesis. Skeletal muscle 17 29047406
2017 Nepetoidin B, a Natural Product, Inhibits LPS-stimulated Nitric Oxide Production via Modulation of iNOS Mediated by NF-κB/MKP-5 Pathways. Phytotherapy research : PTR 15 28504466
2017 Andrographolide inhibits hypoxia-induced hypoxia-inducible factor 1α and endothelin 1 expression through the heme oxygenase 1/CO/cGMP/MKP-5 pathways in EA.hy926 cells. Environmental toxicology 15 29165873
2019 DUSP10 Is a Regulator of YAP1 Activity Promoting Cell Proliferation and Colorectal Cancer Progression. Cancers 14 31717606
2012 An essential function for MKP5 in the formation of oxidized low density lipid-induced foam cells. Cellular signalling 14 22683306
2000 Expression and comparative chromosomal mapping of MKP-5 genes DUSP10/Dusp10. Cytogenetics and cell genetics 14 11060451
2020 The Role of MKP-5 in Adipocyte-Macrophage Interactions during Obesity. Obesity facts 13 31962332
2015 Regulation of Inflammatory Cytokine Production by MKP-5 in Macrophages. Basic & clinical pharmacology & toxicology 12 25615285
2023 Mmu-miR-25-3p promotes macrophage autophagy by targeting DUSP10 to reduce mycobacteria survival. Frontiers in cellular and infection microbiology 10 37256106
2020 Role of MKP-5-p38/MAPK pathway in Clopidogrel-induced gastric mucosal epithelial cells apoptosis and tight junction dysfunction. American journal of translational research 10 32509173
2014 DUSP10 gene polymorphism and risk of colorectal cancer in the Han Chinese population. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) 10 23872954
2015 Polymorphisms in the DUSP10 gene are associated with sex-specific colorectal cancer risk in a Han population. International journal of clinical and experimental pathology 9 25973098
2024 Oroxylin A alleviates myocardial ischemia-reperfusion injury by quelling ferroptosis via activating the DUSP10/MAPK-Nrf2 pathway. Phytotherapy research : PTR 8 39225191
2024 Biomimetic mesenchymal stem cell membrane-coated nanoparticle delivery of MKP5 inhibits hepatic fibrosis through the IRE/XBP1 pathway. Journal of nanobiotechnology 8 39609656
2023 DUSP10 alleviates ischemic stroke-induced neuronal damage by restricting p38/JNK pathway. Behavioural brain research 8 37164190
2022 Defining the structure-activity relationship for a novel class of allosteric MKP5 inhibitors. European journal of medicinal chemistry 8 36116232
2016 p38MAPK activation and DUSP10 expression in meningiomas. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 8 27050915
2015 Mice lacking MKP-1 and MKP-5 Reveal Hierarchical Regulation of Regenerative Myogenesis. Journal of stem cell and regenerative biology 7 27064463
2025 Adipose tissue-derived microRNA-450a-5p induces type 2 diabetes mellitus by downregulating DUSP10. Molecular biomedicine 5 39912972
2020 The mechanism of miR-363-3p/DUSP10 signaling pathway involved in the gastric mucosal injury induced by clopidogrel. Toxicology mechanisms and methods 5 33208005
2025 Microglia-derived extracellular vesicles mediate fine particulate matter-induced Alzheimer's disease-like behaviors through the miR-34a-5p/DUSP10/p-p38 MAPK pathway. Journal of hazardous materials 4 40494244
2024 Nepetoidin B Alleviates Liver Ischemia/Reperfusion Injury via Regulating MKP5 and JNK/P38 Pathway. Drug design, development and therapy 4 38911032
2023 Tumor Promoting Function of DUSP10 in Non-Small Cell Lung Cancer Is Associated With Tumor-Promoting Cytokines. Immune network 4 37670811
2025 Dynamic and structural insights into allosteric regulation on MKP5 a dual-specificity phosphatase. Nature communications 2 40745179
2025 Stem Cell Membrane Biomimetic Nano-Formulation Achieves the Delivery of MKP5 to Ameliorate Diabetic Kidney Disease via the P38 and ERK Pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2 40948363
2024 6-Gingerol attenuates hepatic ischemia/reperfusion injury through regulating MKP5-mediated P38/JNK pathway. Scientific reports 2 38565569
2024 Dynamic and structural insights into allosteric regulation on MKP5 a dual-specificity phosphatase. bioRxiv : the preprint server for biology 2 39282375
2023 DUSP10 is a novel immune-related biomarker connected with survival and cellular proliferation in lower-grade glioma. Aging 2 37387540
2005 [SHP2 and MKP5 in P2Y purinergic receptor-mediated prostate cancer invasion]. Zhonghua bing li xue za zhi = Chinese journal of pathology 2 16181551
2025 Bta-miR-25 alleviates lipopolysaccharide-induced endometritis in cows by targeting DUSP10 to inhibit MAPK signaling. Molecular immunology 1 40815889
2025 The E3 ligase tripartite motif 7 drives the progression of non-alcoholic fatty liver disease by targeting DUSP10 degradation in male mice. Nature communications 1 41290618
2026 Tanshinone IIA prevents septicemia acute kidney injury via regulating the DUSP10/JNK/P38/NLRP3 pathway. American journal of translational research 0 41676308
2025 Mechanisms Underlying the Stimulation of DUSP10/MKP5 Expression in Chondrocytes by High Molecular Weight Hyaluronic Acid. Biomedicines 0 40002789

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