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research
Distinctive Role of KV1.1 Subunits in the Biology and Functions of Low Threshold K+ Channels with Implication for Neurological Disease
Authors
Adelman
Akhtar
+116 more
Ashcroft
Bagchi
Boland
Brew
Brew
Browne
Christie
Clark
Coleman
Cooper
Cox
D'Adamo
Devaux
Dodson
Dodson
Dolly
Eunson
Finol-Urdaneta
Glasscock
Grissmer
Grupe
Gutman
Handforth
Hatton
Heinemann
Herson
Heusser
Hille
Hopkins
Hoshi
Hoshi
Hulme
Hurst
Imbrici
Imredy
Isacoff
Ishii
Jan
Jensen
Jeong
Johnston
Kamb
Kirchheim
Kirizs
Klein
Koch
Kuba
Kullmann
Kullmann
Li
Lodish
London
Long
Manganas
Manganas
Manganas
McIntyre
McNamara
McNamara
Monaghan
Muniz
Nagaya
Norris
Ovsepian
Papazian
Parcej
Pongs
Poujois
Rajakulendran
Rasband
Rasband
Rasband
Rasband
Rea
Rettig
Rhodes
Rhodes
Rhodes
Robbins
Ruppersberg
Schaffer
Scott
Shamotienko
Shamotienko
Sheng
Sheng
Shi
Shook
Smart
Sokolov
Spauschus
Sprunger
Stuhmer
Swanson
Tempel
Tian
Tomlinson
Trimmer
Trimmer
Tytgat
Vacher
Vacher
Vacher
Veh
Wang
Wang
Wang
Wolfart
Yellen
Zerr
Zerr
Zhu
Zhu
Zhu
Zhu
Zuberi
Publication date
26 January 2017
Publisher
'Elsevier BV'
Doi
Cite
Abstract
This document is the Accepted Manuscript version of the following article: Saak V. Ovsepian; Marie LeBerre; Volker Steuber; Valerie B. O’Leary; Christian Leibold; & J. Oliver Dolly; ‘Distinctive role of KV1.1 subunit in the biology and functions of low threshold K+ channels with implications for neurological disease’, Pharmacology & Therapeutics, Vol. 159, March 2016, pp. 93-101. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ The version of record is available on line at doi: http:dx.doi.org/10.1016/j.pharmthera.2016.01.005 © 2016 Elsevier Inc. All rights reserved.The diversity of pore-forming subunits of KV1 channels (KV1.1–KV1.8) affords their physiological versatility and predicts a range of functional impairments resulting from genetic aberrations. Curiously, identified so far human neurological conditions associated with dysfunctions of KV1 channels have been linked exclusively to mutations in the KCNA1 gene encoding for the KV1.1 subunit. The absence of phenotypes related to irregularities in other subunits, including the prevalent KV1.2 subunit of neurons is highly perplexing given that deletion of the corresponding kcna2 gene in mouse models precipitates symptoms reminiscent to those of KV1.1 knockouts. Herein, we critically evaluate the molecular and biophysical characteristics of the KV1.1 protein in comparison with others and discuss their role in the greater penetrance of KCNA1 mutations in humans leading to the neurological signs of episodic ataxia type 1 (EA1). Future research and interpretation of emerging data should afford new insights towards a better understanding of the role of KV1.1 in integrative mechanisms of neurons and synaptic functions under normal and disease conditionsPeer reviewedFinal Accepted Versio
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