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Protein / target

Mitogen-activated protein kinase 10

Encoded byMAPK10P53779Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
5
Clinical candidates
Small-molecule tractable
Druggability
Advanced Clinical
1
Research papers

Protein at a glance

Biological role

Protein serine kinase

Strongest disease association

Gout

Via encoding gene MAPK10 · Genetic evidence · score 0.83

Therapeutic position

Clinically advancing target

Small molecules

Research activity

Emerging research

1 papers · latest 2024

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

Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death.

View complete UniProt function annotation

Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as pro-inflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. Plays regulatory roles in the signaling pathways during neuronal apoptosis. Phosphorylates the neuronal microtubule regulator STMN2. Acts in the regulation of the amyloid-beta precursor protein/APP signaling during neuronal differentiation by phosphorylating APP. Also participates in neurite growth in spiral ganglion neurons. Phosphorylates the CLOCK-BMAL1 heterodimer and plays a role in the photic regulation of the circadian clock (PubMed:22441692). Phosphorylates JUND and this phosphorylation is inhibited in the presence of MEN1 (PubMed:22327296)

Subcellular location

CytoplasmMembraneNucleusMitochondrion
Domains and Gene Ontology detail (19)

Domains & features

Protein kinase

Gene Ontology

  • Ccytoplasm
  • Ccytosol
  • Cmitochondrion
  • Cnucleoplasm
  • Cnucleus
  • Cplasma membrane
  • FATP binding
  • FJUN kinase activity
  • FMAP kinase kinase activity
  • Fprotein serine kinase activity
  • Pcellular senescence
  • PFc-epsilon receptor signaling pathway

464 aa · 53 kDa · 3 isoforms

Biological roles

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

Kinase signallingUniProt · GO
View supporting evidence

Kinase signalling

  • ·Serine/threonine-protein kinase involved in various processes such as neuronal prolifera…
  • ·JUN kinase activity
  • ·MAP kinase kinase activity
  • ·protein serine kinase activity

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 MAPK10

Gene-level evidence surfaced through the gene MAPK10that 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.

Gout
0.83Well supported

Genetic evidence dominant · Open Targets 0.51

Mental Disorders
0.52Moderately supported

Genetic evidence dominant · Open Targets 0.32

Parasitic Diseases
0.51Moderately supported

Genetic evidence dominant · Open Targets 0.31

Osteoarthritis
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

Lennox-Gastaut syndrome
0.40Limited support

Genetic literature evidence dominant · Open Targets 0.27

View evidence synthesis (5)
GoutWell supported
0.83
agreement 0.710.95
Genetic100%

Open Targets aggregate 0.51 · 1 independent evidence family

Mental DisordersModerately supported
0.52
agreement 0.400.64
Genetic100%

Open Targets aggregate 0.32 · 1 independent evidence family

Parasitic DiseasesModerately supported
0.51
agreement 0.390.63
Genetic100%

Open Targets aggregate 0.31 · 1 independent evidence family

OsteoarthritisLimited support
0.48
agreement 0.340.62
Genetic100%Literature0%

Open Targets aggregate 0.29 · 2 independent evidence families

Lennox-Gastaut syndromeLimited support
0.40
agreement 0.260.53
Genetic literature60%Animal model40%

Open Targets aggregate 0.27 · 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
Gout0.51
Mental Disorders0.32
Parasitic Diseases0.31
Osteoarthritis0.29
Lennox-Gastaut syndrome0.27
Nervous System Diseases0.26

Drug development

5 compounds recorded · 5 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (5)
CC-401Phase 2
BRIMAPITIDEPhase 3
TANZISERTIBPhase 2
BRIMAPITIDE, C-TERMINAL ACIDPhase 3
BENTAMAPIMODPhase 2

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small moleculesStrong

Advanced Clinical and Structure with Ligand support this modality.

AntibodiesEmerging

Feasibility evidence (go cc med conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

Other modalitiesStrong

Advanced Clinical support this modality.

View underlying tractability evidence (11)
SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyAB · GO CC med confPR · LiteraturePR · Database UbiquitinationPR · Half-life DataPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2024

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

Most cited

Recent

Europe PMC papers linked directly to this protein.