A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias

Morten S Olesen; Niels Jensen; Anders G Holst; Jonas B Nielsen; Jacob Tfelt-Hansen; Thomas Jespersen; Ahmad Sajadieh; Stig Haunsø; Jens T Lund; Kirstine Calloe; Nicole Schmitt; Jesper Hastrup Svendsen

doi:10.1016/j.cjca.2011.01.003

A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias

Morten S Olesen, Niels Jensen, Anders G Holst, Jonas B Nielsen, Jacob Tfelt-Hansen, Thomas Jespersen, Ahmad Sajadieh, Stig Haunsø, Jens T Lund, Kirstine Calloe, Nicole Schmitt, Jesper Hastrup Svendsen

Hjerteafd. Y

47 Citationer (Scopus)

Abstract

The protein MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is implicated in cardiac arrhythmias.

Originalsprog	Engelsk
Tidsskrift	Canadian Journal of Cardiology
Vol/bind	27
Udgave nummer	4
Sider (fra-til)	523.e17-23
ISSN	0828-282X
DOI	https://doi.org/10.1016/j.cjca.2011.01.003
Status	Udgivet - 2011

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10.1016/j.cjca.2011.01.003

Citationsformater

Olesen, M. S., Jensen, N., Holst, A. G., Nielsen, J. B., Tfelt-Hansen, J., Jespersen, T., Sajadieh, A., Haunsø, S., Lund, J. T., Calloe, K., Schmitt, N., & Svendsen, J. H. (2011). A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias. Canadian Journal of Cardiology, 27(4), 523.e17-23. https://doi.org/10.1016/j.cjca.2011.01.003

Olesen, MS, Jensen, N, Holst, AG, Nielsen, JB , Tfelt-Hansen, J, Jespersen, T, Sajadieh, A , Haunsø, S, Lund, JT, Calloe, K, Schmitt, N & Svendsen, JH 2011, 'A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias', Canadian Journal of Cardiology, bind 27, nr. 4, s. 523.e17-23. https://doi.org/10.1016/j.cjca.2011.01.003

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title = "A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias",

abstract = "The protein MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is implicated in cardiac arrhythmias.",

keywords = "Adult, Atrial Fibrillation, Brugada Syndrome, Codon, Nonsense, Female, Genetic Testing, Humans, Ion Channel Gating, Male, Sodium, Sodium Channels, ran GTP-Binding Protein",

author = "Olesen, {Morten S} and Niels Jensen and Holst, {Anders G} and Nielsen, {Jonas B} and Jacob Tfelt-Hansen and Thomas Jespersen and Ahmad Sajadieh and Stig Hauns{\o} and Lund, {Jens T} and Kirstine Calloe and Nicole Schmitt and Svendsen, {Jesper Hastrup}",

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doi = "10.1016/j.cjca.2011.01.003",

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T1 - A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias

AU - Olesen, Morten S

AU - Jensen, Niels

AU - Holst, Anders G

AU - Nielsen, Jonas B

AU - Tfelt-Hansen, Jacob

AU - Jespersen, Thomas

AU - Sajadieh, Ahmad

AU - Haunsø, Stig

AU - Lund, Jens T

AU - Calloe, Kirstine

AU - Schmitt, Nicole

AU - Svendsen, Jesper Hastrup

PY - 2011

Y1 - 2011

N2 - The protein MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is implicated in cardiac arrhythmias.

AB - The protein MOG1 is a cofactor of the cardiac sodium channel, Nav1.5. Overexpression of MOG1 in Nav1.5-expressing cells increases sodium current markedly. Mutations in the genes encoding Nav1.5 and its accessory proteins have been associated with cardiac arrhythmias of significant clinical impact. We sought to investigate whether MOG1 is implicated in cardiac arrhythmias.

KW - Adult

KW - Atrial Fibrillation

KW - Brugada Syndrome

KW - Codon, Nonsense

KW - Female

KW - Genetic Testing

KW - Humans

KW - Ion Channel Gating

KW - Male

KW - Sodium

KW - Sodium Channels

KW - ran GTP-Binding Protein

U2 - 10.1016/j.cjca.2011.01.003

DO - 10.1016/j.cjca.2011.01.003

M3 - Journal article

C2 - 21621375

SN - 0828-282X

VL - 27

SP - 523.e17-23

JO - Canadian Journal of Cardiology

JF - Canadian Journal of Cardiology

IS - 4

ER -

A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias

Abstract

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