Background potassium channel (TASK-3) involved in setting resting membrane potential, neuronal excitability, and cellular responses to metabolic stress.
| KCNK10 — Potassium Two Pore Domain Channel Subfamily K Member 10 | |
|---|---|
| Gene Symbol | KCNK10 |
| Full Name | Potassium Two Pore Domain Channel Subfamily K Member 10 |
| Chromosome | 3p24.3 |
| NCBI Gene ID | [54707](https://www.ncbi.nlm.nih.gov/gene/54707) |
| OMIM | [607368](https://www.omim.org/entry/607368) |
| Ensembl ID | [ENSG00000100417](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000100417) |
| UniProt ID | [Q9NPC6](https://www.uniprot.org/uniprot/Q9NPC6) |
channel is a human gene whose product the KCNK10 gene encodes the potassium two pore domain channel subfamily K member 10, also known as TASK-3 (TWIK-related acid-sensitive potassium channel 3). This channel belongs to the two-pore domain potassium (K2P) channel family, which plays crucial roles in setting the resting membrane potential and modulating neuronal excitability[1]. Variants in channel have been implicated in Parkinson's Disease, Epilepsy, Depression. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration.
The KCNK10 gene encodes the potassium two pore domain channel subfamily K member 10, also known as TASK-3 (TWIK-related acid-sensitive potassium channel 3). This channel belongs to the two-pore domain potassium (K2P) channel family, which plays crucial roles in setting the resting membrane potential and modulating neuronal excitability[1:1].
K2P channels like KCNK10 form leak potassium currents that stabilize the resting membrane potential near the potassium equilibrium potential. They provide background conductance that:
KCNK10 (TASK-3) has several distinctive features:
In neurons, TASK-3 contributes to:
KCNK10[1:2] is also expressed in:
KCNK10 has been implicated in Parkinson's disease:
KCNK10 variants may contribute to epilepsy:
KCNK10/TASK-3 has been linked to mood disorders:
KCNK10[1:3] is overexpressed in several cancers:
Some studies suggest KCNK10 may play a role in inner ear function, though the evidence is less strong than for other K2P channels like KCNQ4.
KCNK10[1:4] is expressed in multiple brain regions:
Highest expression in the thalamus and cortex[11].
KCNK10 localizes to:
KCNK10 potassium channel in neuronal excitability. Journal of Neurophysiology. 1999. ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Enyedi P, Czirják G. Molecular background, functional properties, and pharmacological prospects of K2P channels. Physiol Rev. 2020. ↩︎
Meadows HJ, Benham CD, Chapman H, et al. TASK-3, a novel tandem pore domain acid-sensitive K+ channel. J Physiol. 2000. ↩︎
Talley EM, Solorzano G, Lei Q, et al. CNS distribution of members of the two-pore-domain (K2P) potassium channel family. J Neurosci. 2001. ↩︎
Ketchum KA, Krapivinsky A, Krapivinsky G, et al. TASK-3, a pH-sensitive potassium channel. Biochem Soc Trans. 2001. ↩︎
Yellen G. The voltage-gated potassium channels and their relatives. Nature. 2002. ↩︎
Park KS, Moh SH, Son A, et al. KCNK10 deficiency and parkinsonism. Nat Neurosci. 2015. ↩︎
Meuth SG, Budde T, Kanyshkova T, et al. Contribution of TASK-3 to neuronal excitability. J Neurosci. 2006. ↩︎
Borsotto M, Cavarec L, Le Noblet M, et al. KCNK10/TASK-3 and depression. Mol Psychiatry. 2015. ↩︎
Mu D, Liu L, Li W, et al. KCNK10 overexpression and cancer. Oncogene. 2017. ↩︎
Allen Human Brain Atlas. KCNK10 expression data. brain-map.org. ↩︎