Protein / target
ATP-sensitive inward rectifier potassium channel 10
Protein at a glance
Biological role
ATP-activated inward rectifier potassium channel
Strongest disease association
Genetic Diseases, Inborn
Research activity
Emerging research
Derived from structured UniProt, Open Targets and literature data on this page.
Protein profile
Canonical identity and biological annotation from UniProt.
Function overview
May be responsible for potassium buffering action of glial cells in the brain.
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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
Domains and Gene Ontology detail (14)Hide
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
Biological roles
What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.
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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
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.
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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.
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Tractability
Small molecules — Emerging
Antibodies — Emerging
Protein degraders — Emerging
View underlying tractability evidence (5)Hide
Raw Open Targets tractability assessment buckets, by modality.
Research activity
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.