GO curators for mouse genes have assigned the following annotations to the gene product of Kcnq4. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene forms a potassium channel that is thought to play a critical role in the regulation of neuronal excitability, particularly in sensory cells of the cochlea. The current generated by this channel is inhibited by M1 muscarinic acetylcholine receptors and activated by retigabine, a novel anti-convulsant drug. The encoded protein can form a homomultimeric potassium channel or possibly a heteromultimeric channel in association with the protein encoded by the KCNQ3 gene. Defects in this gene are a cause of nonsyndromic sensorineural deafness type 2 (DFNA2), an autosomal dominant form of progressive hearing loss. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Kcnq4
participates in the following biological processes:
Kharkovets T et al. (2006) Mice with altered KCNQ4 K+ channels implicate sensory outer hair cells in human progressive deafness. EMBO J, 25:642-52. (PubMed:16437162)