Literature DB >> 33860384

Kv7 Channels and Excitability Disorders.

Frederick Jones1, Nikita Gamper2,3, Haixia Gao4.   

Abstract

Kv7.1-Kv7.5 (KCNQ1-5) K+ channels are voltage-gated K+ channels with major roles in neurons, muscle cells and epithelia where they underlie physiologically important K+ currents, such as neuronal M current and cardiac IKs. Specific biophysical properties of Kv7 channels make them particularly well placed to control the activity of excitable cells. Indeed, these channels often work as 'excitability breaks' and are targeted by various hormones and modulators to regulate cellular activity outputs. Genetic deficiencies in all five KCNQ genes result in human excitability disorders, including epilepsy, arrhythmias, deafness and some others. Not surprisingly, this channel family attracts considerable attention as potential drug targets. Here we will review biophysical properties and tissue expression profile of Kv7 channels, discuss recent advances in the understanding of their structure as well as their role in various neurological, cardiovascular and other diseases and pathologies. We will also consider a scope for therapeutic targeting of Kv7 channels for treatment of the above health conditions.
© 2021. The Author(s), under exclusive license to Springer Nature Switzerland AG.

Entities:  

Keywords:  Channelopathy; Epilepsy; KCNQ; Kv7 channel; M current; Pain

Mesh:

Substances:

Year:  2021        PMID: 33860384     DOI: 10.1007/164_2021_457

Source DB:  PubMed          Journal:  Handb Exp Pharmacol        ISSN: 0171-2004


  329 in total

1.  A mutually induced conformational fit underlies Ca2+-directed interactions between calmodulin and the proximal C terminus of KCNQ4 K+ channels.

Authors:  Crystal R Archer; Benjamin T Enslow; Alexander B Taylor; Victor De la Rosa; Akash Bhattacharya; Mark S Shapiro
Journal:  J Biol Chem       Date:  2019-02-26       Impact factor: 5.157

2.  Expression and motor functional roles of voltage-dependent type 7 K(+) channels in the human taenia coli.

Authors:  Alice Adduci; Maria Martire; Maurizio Taglialatela; Vincenzo Arena; Gianluca Rizzo; Claudio Coco; Diego Currò
Journal:  Eur J Pharmacol       Date:  2013-10-10       Impact factor: 4.432

3.  Novel exon 1 protein-coding regions N-terminally extend human KCNE3 and KCNE4.

Authors:  Geoffrey W Abbott
Journal:  FASEB J       Date:  2016-05-09       Impact factor: 5.191

4.  Overview of Basic Mechanisms of Cardiac Arrhythmia.

Authors:  Charles Antzelevitch; Alexander Burashnikov
Journal:  Card Electrophysiol Clin       Date:  2011-03-01

5.  KCNE5 induces time- and voltage-dependent modulation of the KCNQ1 current.

Authors:  Kamilla Angelo; Thomas Jespersen; Morten Grunnet; Morten Schak Nielsen; Dan A Klaerke; Søren-Peter Olesen
Journal:  Biophys J       Date:  2002-10       Impact factor: 4.033

6.  Reduction of spike frequency adaptation and blockade of M-current in rat CA1 pyramidal neurones by linopirdine (DuP 996), a neurotransmitter release enhancer.

Authors:  S P Aiken; B J Lampe; P A Murphy; B S Brown
Journal:  Br J Pharmacol       Date:  1995-08       Impact factor: 8.739

7.  Molecular expression and pharmacological evidence for a functional role of kv7 channel subtypes in Guinea pig urinary bladder smooth muscle.

Authors:  Serge A Y Afeli; John Malysz; Georgi V Petkov
Journal:  PLoS One       Date:  2013-09-20       Impact factor: 3.240

8.  Functional expression of KCNQ (Kv7) channels in guinea pig bladder smooth muscle and their contribution to spontaneous activity.

Authors:  U A Anderson; C Carson; L Johnston; S Joshi; A M Gurney; K D McCloskey
Journal:  Br J Pharmacol       Date:  2013-07       Impact factor: 8.739

9.  Role of KCNQ potassium channels in stress-induced deficit of working memory.

Authors:  Amy F T Arnsten; Lu E Jin; Nao J Gamo; Brian Ramos; Constantinos D Paspalas; Yury M Morozov; Anna Kata; Nigel S Bamford; Mark F Yeckel; Leonard K Kaczmarek; Lynda El-Hassar
Journal:  Neurobiol Stress       Date:  2019-07-26
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  4 in total

1.  Evidence for Dual Activation of IK(M) and IK(Ca) Caused by QO-58 (5-(2,6-Dichloro-5-fluoropyridin-3-yl)-3-phenyl-2-(trifluoromethyl)-1H-pyrazolol[1,5-a]pyrimidin-7-one).

Authors:  Chao-Liang Wu; Poyuan Fu; Hsin-Yen Cho; Tzu-Hsien Chuang; Sheng-Nan Wu
Journal:  Int J Mol Sci       Date:  2022-06-24       Impact factor: 6.208

2.  Gain of function due to increased opening probability by two KCNQ5 pore variants causing developmental and epileptic encephalopathy.

Authors:  Mario Nappi; Vincenzo Barrese; Lidia Carotenuto; Gaetan Lesca; Audrey Labalme; Dorothee Ville; Thomas Smol; Mélanie Rama; Anne Dieux-Coeslier; Clotilde Rivier-Ringenbach; Maria Virginia Soldovieri; Paolo Ambrosino; Ilaria Mosca; Michael Pusch; Francesco Miceli; Maurizio Taglialatela
Journal:  Proc Natl Acad Sci U S A       Date:  2022-04-04       Impact factor: 12.779

3.  Clinically Relevant KCNQ1 Variants Causing KCNQ1-KCNE2 Gain-of-Function Affect the Ca2+ Sensitivity of the Channel.

Authors:  Christiane K Bauer; Tess Holling; Denise Horn; Mário Nôro Laço; Ebtesam Abdalla; Omneya Magdy Omar; Malik Alawi; Kerstin Kutsche
Journal:  Int J Mol Sci       Date:  2022-08-26       Impact factor: 6.208

4.  Repressor element 1-silencing transcription factor deficiency yields profound hearing loss through Kv7.4 channel upsurge in auditory neurons and hair cells.

Authors:  Haiwei Zhang; Hongchen Li; Mingshun Lu; Shengnan Wang; Xueya Ma; Fei Wang; Jiaxi Liu; Xinyu Li; Haichao Yang; Fan Zhang; Haitao Shen; Noel J Buckley; Nikita Gamper; Ebenezer N Yamoah; Ping Lv
Journal:  Elife       Date:  2022-09-20       Impact factor: 8.713

  4 in total

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