Aliases for KCNQ5 Gene
External Ids for KCNQ5 Gene
Previous GeneCards Identifiers for KCNQ5 Gene
This gene is a member of the KCNQ potassium channel gene family that is differentially expressed in subregions of the brain and in skeletal muscle. The protein encoded by this gene yields currents that activate slowly with depolarization and can form heteromeric channels with the protein encoded by the KCNQ3 gene. Currents expressed from this protein have voltage dependences and inhibitor sensitivities in common with M-currents. They are also inhibited by M1 muscarinic receptor activation. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2009]
GeneCards Summary for KCNQ5 Gene
KCNQ5 (Potassium Voltage-Gated Channel Subfamily Q Member 5) is a Protein Coding gene. Diseases associated with KCNQ5 include Mental Retardation, Autosomal Dominant 46 and Autosomal Dominant Non-Syndromic Intellectual Disability. Among its related pathways are Circadian entrainment and Celecoxib Pathway, Pharmacodynamics. Gene Ontology (GO) annotations related to this gene include ion channel activity and delayed rectifier potassium channel activity. An important paralog of this gene is KCNQ4.
UniProtKB/Swiss-Prot Summary for KCNQ5 Gene
Associates with KCNQ3 to form a potassium channel which contributes to M-type current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons. Therefore, it is important in the regulation of neuronal excitability. May contribute, with other potassium channels, to the molecular diversity of a heterogeneous population of M-channels, varying in kinetic and pharmacological properties, which underlie this physiologically important current. Insensitive to tetraethylammonium, but inhibited by barium, linopirdine and XE991. Activated by niflumic acid and the anticonvulsant retigabine. As the native M-channel, the potassium channel composed of KCNQ3 and KCNQ5 is also suppressed by activation of the muscarinic acetylcholine receptor CHRM1.