Molecular genetics and functional anomalies in a series of 248 Brugada cases with 11 mutations in the TRPM4 channel (Q28485378)

11

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Ninda Syam

4

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Vincent Probst

object named as

Vincent Probst

6

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author name string

Hui Liu

1

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Stéphanie Chatel

2

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Christophe Simard

3

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Laurent Salle

5

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Julie Morel

7

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Gilles Millat

8

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Michel Lopez

9

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Romain Guinamard

12

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Patrice Bouvagnet

Creative Commons Attribution 4.0 International

13

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language of work or name

English

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publication date

2013

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published in

PLOS One

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volume

8

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page(s)

e54131

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issue

1

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copyright license

start time

30 January 2013

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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cites work

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Impaired endocytosis of the ion channel TRPM4 is associated with human progressive familial heart block type I

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TRPM4 is a Ca2+-activated nonselective cation channel mediating cell membrane depolarization

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Amino acid difference formula to help explain protein evolution

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Increased catecholamine secretion contributes to hypertension in TRPM4-deficient mice

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Crossref

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0054131

Gain-of-function mutations in TRPM4 cause autosomal dominant isolated cardiac conduction disease.

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Mutational spectrum in the Ca(2+)--activated cation channel gene TRPM4 in patients with cardiac conductance disturbances

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Supernormal excitability and conduction in the His-Purkinje system of the dog

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Right ventricular histological substrate and conduction delay in patients with Brugada syndrome

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Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium

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10.1371/JOURNAL.PONE.0054131

Identifiers

DOI

1 reference

1469281

ADS bibcode

2013PLoSO...854131L

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1469281

1 reference

1 reference

1 reference