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Potassium voltage-gated channel, KQT-like subfamily, member 4

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] (from NCBI)
Top mentioned proteins: KCNQ1, HAIR, KCNQ2, CAN, HAD
Papers on KCNQ4
KCNQ Potassium Channels Modulate Sensitivity of Skin D-hair Mechanoreceptors.
Jentsch et al., Delbrück, Germany. In J Biol Chem, Feb 2016
Together with previous work on the specific role of KCNQ4 in rapidly adapting skin mechanoreceptors, our results show that different KCNQ isoforms are specifically expressed in particular subsets of mechanosensory neurons and modulate their sensitivity directly in sensory nerve endings.
Transient alteration of the vestibular calyceal junction and synapse in response to chronic ototoxic insult in rats.
Llorens et al., l'Hospitalet de Llobregat, Spain. In Dis Model Mech, Nov 2015
KCNQ4 was mislocalized during intoxication and recovered control-like localization after washout.
A novel frameshift mutation in KCNQ4 in a family with autosomal recessive non-syndromic hearing loss.
Matsunaga et al., Tokyo, Japan. In Biochem Biophys Res Commun, Sep 2015
Mutation of KCNQ4 has been reported to cause autosomal dominant non-syndromic hearing loss (DFNA2A) that usually presents as progressive hearing loss starting from mild to moderate hearing loss during childhood.
Potent KCNQ2/3-specific channel activator suppresses in vivo epileptic activity and prevents the development of tinnitus.
Tzounopoulos et al., Pittsburgh, United States. In J Neurosci, Jul 2015
Moreover, unlike retigabine, SF0034 did not shift the voltage dependence of either KCNQ4 or KCNQ5 homomeric channels.
Potassium channel activator attenuates salicylate-induced cochlear hearing loss potentially ameliorating tinnitus.
Salvi et al., Buffalo, United States. In Front Neurol, 2014
Salicylate-induced hearing loss is believed to arise from a reduction in the electromotile response of outer hair cells (OHCs) and/or reduction of KCNQ4 potassium currents in OHCs, which decreases the driving force for the transduction current.
Overexpression of tau downregulated the mRNA levels of Kv channels and improved proliferation in N2A cells.
Hao et al., Wuhan, China. In Plos One, 2014
This treatment led to a downregulation of mRNA levels of several Kv channels, including Kv2.1, Kv3.1, Kv4.1, Kv9.2, and KCNH4, but no significant alteration was observed for Kv5.1 and KCNQ4.
The Role of the Carboxyl Terminus Helix C-D Linker in Regulating KCNQ3 K+ Current Amplitudes by Controlling Channel Trafficking.
Shapiro et al., San Antonio, United States. In Plos One, 2014
KCNQ3 homomers yield much smaller currents compared to KCNQ2 or KCNQ4 homomers and KCNQ2/3 heteromers.
[Personalized molecular medicine: new paradigms in the treatment of cochlear implant and cancer patients].
Röcken et al., Tübingen, Germany. In Hno, 2014
RESULTS: Personalized medicine based on molecular-genetic evaluation of functional proteins such as otoferlin, connexin 26 and KCNQ4 or the Usher gene is becoming increasingly important for the indication of CI in the context of infant deafness.
Contribution of genetic factors to noise-induced hearing loss: a human studies review.
Pawelczyk et al., Łódź, Poland. In Mutat Res, 2013
So far, the most promising results were obtained for two genes encoding potassium ion channels (KCNQ4 and KCNE1), catalase (CAT), protocadherin 15 (PCDH15), myosin 14 (MYH14) and heat shock protein (HSP70), because they were replicated in two (Polish and Swedish) or three (Polish, Swedish and Chinese) populations, and were sufficient in size to yield high power for the detection of a causative allele.
Regulation of ion channels by the serum- and glucocorticoid-inducible kinase SGK1.
Shumilina et al., Tübingen, Germany. In Faseb J, 2013
SGK1 activates a wide variety of ion channels (e.g., ENaC, SCN5A, TRPV4-6, ROMK, Kv1.3, Kv1.5, Kv4.3, KCNE1/KCNQ1, KCNQ4, ASIC1, GluR6, ClCKa/barttin, ClC2, CFTR, and Orai/STIM), which participate in the regulation of transport, hormone release, neuroexcitability, inflammation, cell proliferation, and apoptosis.
KCNQ4 K(+) channels tune mechanoreceptors for normal touch sensation in mouse and man.
Lewin et al., Berlin, Germany. In Nat Neurosci, 2012
This work describes a gene mutation that modulates touch sensitivity in mice and humans and establishes KCNQ4 as a specific molecular marker for rapidly adapting Meissner and a subset of hair follicle afferents.
Identification of a novel, small molecule activator of KCNQ1 channels
Li et al., Bethesda, United States. In Unknown Journal, 2012
ML277 was identified as a potent (EC50 = 0.26 μM) activator of KCNQ1 channels with more than 100-fold selectivity for activation of KCNQ1 channels compared with closely related KCNQ2 and KCNQ4 channels and with distantly related hERG potassium channels.
Gene localization in a Chinese family with autosomal dominant non-syndromic deafness.
He et al., Taiwan. In Acta Otolaryngol, 2011
no sequence alterations that segregate with autosomal dominant non-syndromic deafness in either GJB3 or KCNQ4
Novel expression and regulation of voltage-dependent potassium channels in placentas from women with preeclampsia.
Tribe et al., London, United Kingdom. In Hypertension, 2011
Data show that KCNQ4 and KCNE1 isoforms were suppressed in placentas from term preeclamptic women.
Downregulation of Kv7.4 channel activity in primary and secondary hypertension.
Greenwood et al., London, United Kingdom. In Circulation, 2011
In 2 different rat and mouse models of hypertension, the functional impact of Kv7 channels was dramatically downregulated.
A small molecule activator of KCNQ2 and KCNQ4 channels
Li et al., Bethesda, United States. In Unknown Journal, 2011
EC50 = 230 nM) and KCNQ4 (Kv7.4,
K(V)7/KCNQ channels are functionally expressed in oligodendrocyte progenitor cells.
He et al., Shanghai, China. In Plos One, 2010
Findings show that K(V)7/KCNQ channels were functionally expressed in primary cultured OLCs and might play an important role in OPCs functioning in physiological or pathological conditions.
Deafness and renal tubular acidosis in mice lacking the K-Cl co-transporter Kcc4.
Jentsch et al., Hamburg, Germany. In Nature, 2002
K(+) probably exits outer hair cells by KCNQ4 K(+) channels(), and is then transported by means of a gap junction system connecting supporting Deiters' cells and fibrocytes() back to the stria vascularis.
A constitutively open potassium channel formed by KCNQ1 and KCNE3.
Jentsch et al., Hamburg, Germany. In Nature, 2000
It also suppresses the currents of KCNQ4 and HERG potassium channels.
KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness.
Jentsch et al., Hamburg, Germany. In Cell, 1999
A mutation in this gene in a DFNA2 pedigree changes a residue in the KCNQ4 pore region.
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