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Protein / target

ATP-sensitive inward rectifier potassium channel 10

Encoded byKCNJ10P78508Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Druggable Family
2
Research papers

Protein at a glance

Biological role

ATP-activated inward rectifier potassium channel

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene KCNJ10 · Genetic evidence · score 0.62

Research activity

Emerging research

2 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

May be responsible for potassium buffering action of glial cells in the brain.

View complete UniProt function annotation

May be responsible for potassium buffering action of glial cells in the brain (By similarity). Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it (PubMed:8995301). Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages (PubMed:8995301). The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium (PubMed:8995301). In the kidney, together with KCNJ16, mediates basolateral K(+) recycling in distal tubules; this process is critical for Na(+) reabsorption at the tubules (PubMed:24561201)

Subcellular location

MembraneBasolateral cell membrane
Domains and Gene Ontology detail (14)

Gene Ontology

  • Castrocyte projection
  • Cbasolateral plasma membrane
  • Ccell body
  • Cciliary base
  • Cmonoatomic ion channel complex
  • Cplasma membrane
  • FATP binding
  • FATP-activated inward rectifier potassium channel activity
  • Finward rectifier potassium channel activity
  • Pcellular response to potassium ion
  • Pnon-motile cilium assembly
  • Ppotassium ion import across plasma membrane

379 aa · 43 kDa

Biological roles

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

Ion channel gatingGO
View supporting evidence

Ion channel gating

  • ·monoatomic ion channel complex
  • ·potassium ion transmembrane transport

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 KCNJ10

Gene-level evidence surfaced through the gene KCNJ10that 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.

Genetic Diseases, Inborn
0.62Moderately supported

Genetic evidence dominant · Open Targets 0.38

Cerebellar Ataxia
0.59Moderately supported

Genetic evidence dominant · Open Targets 0.35

Nonsyndromic genetic hearing loss
0.49Limited support

Genetic literature evidence dominant · Open Targets 0.37

View evidence synthesis (3)
Genetic Diseases, InbornModerately supported
0.62
agreement 0.480.76
Genetic99%Literature1%

Open Targets aggregate 0.38 · 2 independent evidence families

Cerebellar AtaxiaModerately supported
0.59
agreement 0.450.73
Genetic86%Literature14%

Open Targets aggregate 0.35 · 2 independent evidence families

Nonsyndromic genetic hearing lossLimited support
0.49
agreement 0.330.64
Genetic literature100%

Open Targets aggregate 0.37 · 1 independent evidence family

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
Genetic Diseases, Inborn0.38
Nonsyndromic genetic hearing loss0.37
Cerebellar Ataxia0.35

Tractability

Small moleculesEmerging

Feasibility evidence (druggable family) — no clinical-stage drug of this modality recorded.

AntibodiesEmerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

View underlying tractability evidence (5)
SM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 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.