Ask about this productRelated genes to: KCNA10 Blocking Peptide
- Gene:
- KCNA10 NIH gene
- Name:
- potassium voltage-gated channel subfamily A member 10
- Previous symbol:
- -
- Synonyms:
- Kv1.8
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-19
- Date modifiied:
- 2016-10-05
Related products to: KCNA10 Blocking Peptide
Related articles to: KCNA10 Blocking Peptide
- Exposure of mammals to ototoxic compounds causes hair cell (HC) loss in the vestibular sensory epithelia of the inner ear. In chronic exposure models, this loss often occurs by extrusion of the HC from the sensory epithelium towards the luminal cavity. HC extrusion is preceded by several steps that begin with detachment and synaptic uncoupling of the cells from the afferent terminals of their postsynaptic vestibular ganglion neurons. The purpose of this study was to identify gene expression mechanisms that drive these responses to chronic ototoxic stress. - Source: PubMed
Publication date: 2025/09/04
Borrajo MireiaGreguske Erin AMaroto Alberto FPalou AïdaRenner AnaGiménez-Esbrí VíctorSedano DavidGut MartaEsteve-Codina AnnaMartín-Mur BeatrizBarrallo-Gimeno AlejandroLlorens Jordi - The number of individuals diagnosed with opioid use disorder (OUD) has risen steeply because of increased prescribing of opioid drugs including oxycodone for chronic pain relief. When rats given extended access to oxycodone only a subset of animals self-administers more drug over time. Identifying the molecular mechanism associated with this behavior can introduce novel ways to combat OUD. Herein, we sought to identify the alteration in the expression of voltage gated and calcium activated potassium channels after extended access to oxycodone self-administration. - Source: PubMed
Publication date: 2025/08/11
Wabreha Ammanuel YAdjei NasserLadenheim BruceCadet Jean LudDaiwile Atul P - Chronic dry cough is a symptom of common lung conditions, can occur as a side-effect of angiotensin-converting enzyme inhibitors (ACEis), or may be unexplained. Despite the substantial health burden presented by chronic dry cough, its biological mechanisms remain unclear. We hypothesised shared genetic architecture between chronic dry cough and ACEi-induced cough and aimed to identify causal genes underlying both phenotypes. - Source: PubMed
Publication date: 2025/09/25
Coley KayeshaJohn CatherineGhouse JonasShepherd David JShrine NickIzquierdo Abril GKanoni StavroulaMagavern Emma FPacker RichardMcGarvey LorcanSmith Jaclyn ABundgaard HenningOstrowski Sisse RErikstrup ChristianPedersen Ole B Vvan Heel David A Hennah WilliamMarttila MikkoFree Robert CHollox Edward JWain Louise VTobin Martin DBatini Chiara - Lung function deficits may be caused by early life epigenetic programming. Early childhood studies are necessary to understand life-course trends in lung diseases. - Source: PubMed
Publication date: 2025/05/14
Kachroo PriyadarshiniShutta Katherine HMaiorino EnricoMoll MatthewHecker JulianCarey VincentMcGeachie Michael JLitonjua Augusto ACeledón Juan C Weiss Scott TDeMeo Dawn L - Vestibular hair cells (HCs) faithfully and rapidly detect head motions and gravity, driving motor reflexes that stabilize balance and gaze during locomotion. With the transition from water to land, the amniote vestibular inner ear added type I HCs, which differ from amniote type II HCs and anamniote HCs by their large calyx afferent synapse, non-quantal afferent transmission, and a large, low-voltage-activated K conductance (g). We recently showed that both g and the major type II K conductances (A-type and delayed rectifier) require K1.8 () subunits. Here we compared K1.8-null ( ) and control animals to see how K1.8 affects function as measured by receptor potentials and nonquantal postsynaptic potentials evoked by direct hair bundle motions, and by vestibulomotor behaviors. Recordings were taken from extrastriolar zones of the utricle. In both HC types, K1.8 affected receptor potentials by reducing response time and gain, increasing dampening, and expanding the frequency bandwidth toward high frequencies. Effects are most prominent in type I HCs: lowpass corner frequencies of receptor potentials in HCs of both types were ~20 Hz, . ~400 Hz in control type I and ~70 Hz in control type II. We recorded nonquantal postsynaptic potentials from extrastriolar calyces, and found that the synaptic transfer function had lower gain and greater phase lag in mice. In behavioral tests, mice had vestibular-ocular reflexes with different response dynamics at low frequencies, impaired performance on a narrow balance beam, abnormal body posture and abnormal head motions in water and on land, and also rarely assumed bipedal stances. These vestibulomotor deficits in mice likely reflect the changes noted in HCs, where K1.8 expression is concentrated; that is, slower signaling of high-frequency head motions by HCs fails to fully stabilize body and head position during locomotion. Thus, g (K1.8) contributes to fast signal transmission in the amniote vestibular inner ear and supports improved performance on challenging vestibulomotor tasks. - Source: PubMed
Publication date: 2025/01/28
Martin Hannah RVerdone Brandie MorrisLópez-Ramírez OmarGreen MerrillSilvian DanaScott EmilyCullen Kathleen EEatock Ruth Anne