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Protein / target

Dual specificity protein phosphatase 1

Encoded byDUSP1P28562Homo sapiensSwiss-Prot
UniProt: P28562Ensembl: ENSG00000120129HGNC: HGNC:3064NCBI Gene: 1843
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

MAP kinase tyrosine/serine/threonine phosphatase

Strongest disease association

Glaucoma

Via encoding gene DUSP1 · Genetic evidence · score 0.57

Research activity

Emerging research

1 papers · latest 2000

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Dual specificity phosphatase that dephosphorylates MAP kinase MAPK1/ERK2 on both 'Thr-183' and 'Tyr-185', regulating its activity during the meiotic cell cycle

Subcellular location

Nucleus
Domains and Gene Ontology detail (36)

Domains & features

RhodaneseTyrosine-protein phosphatase

Gene Ontology

  • Ccytoplasm
  • Cnucleus
  • Fgrowth factor binding
  • FMAP kinase tyrosine/serine/threonine phosphatase activity
  • Fmitogen-activated protein kinase binding
  • Fphosphoprotein phosphatase activity
  • Fprotein serine/threonine phosphatase activity
  • Fprotein tyrosine phosphatase activity
  • Fprotein tyrosine/serine/threonine phosphatase activity
  • Pcellular response to chemokine
  • Pcellular response to hormone stimulus
  • Pendoderm formation

367 aa · 39 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Cell proliferation & survivalGOCell migrationGOCell-cycle regulationGOApoptosis & cell deathGO
View supporting evidence

Cell proliferation & survival

  • ·negative regulation of cell population proliferation

Cell migration

  • ·negative regulation of monocyte chemotaxis

Cell-cycle regulation

  • ·regulation of mitotic cell cycle spindle assembly checkpoint

Apoptosis & cell death

  • ·negative regulation of apoptotic process
  • ·positive regulation of apoptotic process

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene DUSP1

Gene-level evidence surfaced through the gene DUSP1 that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Glaucoma
0.57Moderately supported

Genetic evidence dominant · Open Targets 0.35

Glaucoma, Open-Angle
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

Nervous System Diseases
0.45Limited support

Genetic evidence dominant · Open Targets 0.27

Herpes Zoster
0.44Limited support

Genetic evidence dominant · Open Targets 0.27

Dermatitis, Atopic
0.43Limited support

Genetic evidence dominant · Open Targets 0.26

View evidence synthesis (5)
GlaucomaModerately supported
0.57
agreement 0.45–0.69
Genetic100%

Open Targets aggregate 0.35 · 1 independent evidence family

Glaucoma, Open-AngleLimited support
0.48
agreement 0.34–0.61
Genetic99%Literature1%

Open Targets aggregate 0.29 · 2 independent evidence families

Nervous System DiseasesLimited support
0.45
agreement 0.31–0.58
Genetic97%Literature3%

Open Targets aggregate 0.27 · 2 independent evidence families

Herpes ZosterLimited support
0.44
agreement 0.32–0.56
Genetic100%

Open Targets aggregate 0.27 · 1 independent evidence family

Dermatitis, AtopicLimited support
0.43
agreement 0.29–0.57
Genetic97%Literature3%

Open Targets aggregate 0.26 · 2 independent evidence families

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Neurodegenerative Diseases0.45
Glaucoma0.35
Glaucoma, Open-Angle0.29
Nervous System Diseases0.27
Herpes Zoster0.27
Dermatitis, Atopic0.26
Placental abruption0.14
Carcinoma, Non-Small-Cell Lung0.11

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (5)
SM · Structure with LigandSM · High-Quality LigandPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2000

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

The MAPK/ERK cascade targets both Elk-1 and cAMP response element-binding protein to control long-term potentiation-dependent gene expression in the dentate gyrus in vivo.494 cites

Davis S · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000

Recent

The MAPK/ERK cascade targets both Elk-1 and cAMP response element-binding protein to control long-term potentiation-dependent gene expression in the dentate gyrus in vivo.

Davis S · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000

Europe PMC papers linked directly to this protein.