ArticleThe Journal of general physiology2015
Identification of a key residue in Kv7.1 potassium channel essential for sensing external potassium ions.
Article in The Journal of general physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Molecular differences between young and mature stria vascularis from organotypic explants and transcriptomics.iScience · 2025Article
- Mechanism of external K+ sensitivity of KCNQ1 channels.The Journal of general physiology · 2023Article
- Sensing its own permeant ion: KCNQ1 channel inhibition by external K.The Journal of general physiology · 2023Article
- KCNE1 tunes the sensitivity of KeLife · 2018Article
- Possible mechanisms for sensorineural hearing loss and deafness in patients with propionic acidemia.Orphanet journal of rare diseases · 2017Article
- A novel missense mutation in the C2C domain of otoferlin causes profound hearing impairment in an Omani family with auditory neuropathy.Saudi medical journal · 2016Article
- The Role of KV7.3 in Regulating Osteoblast Maturation and Mineralization.International journal of molecular sciences · 2016Article
- KCNK5 channels mostly expressed in cochlear outer sulcus cells are indispensable for hearing.Nature communications · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Kv7.1 voltage-gated K(+) (Kv) channels are present in the apical membranes of marginal cells of the stria vascularis of the inner ear, where they mediate K(+) efflux into the scala media (cochlear duct) of the cochlea. As such, they are exposed to the K(+)-rich (∼ 150 mM of external K(+) (K(+) e)) environment of the endolymph. Previous studies have shown that Kv7.1 currents are substantially suppressed by high K(+) e (independent of the effects of altering the electrochemical gradient). However, the molecular basis for this inhibition, which is believed to involve stabilization of an inactivated state, remains unclear. Using sequence alignment of S5-pore linkers of several Kv channels, we identified a key residue, E290, found in only a few Kv channels including Kv7.1. We used substituted cysteine accessibility methods and patch-clamp analysis to provide evidence that the ability of Kv7.1 to sense K(+) e depends on E290, and that the charge at this position is essential for Kv7.1's K(+) e sensitivity. We propose that Kv7.1 may use this feedback mechanism to maintain the magnitude of the endocochlear potential, which boosts the driving force to generate the receptor potential of hair cells. The implications of our findings transcend the auditory system; mutations at this position also result in long QT syndrome in the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.