Loss-of-Function of the Voltage-Gated Sodium Channel NaV1.5 (Channelopathies) in Patients With Irritable Bowel Syndrome - Wikidata - wikimedia - TriplyDB

Loss-of-Function of the Voltage-Gated Sodium Channel NaV1.5 (Channelopathies) in Patients With Irritable Bowel Syndrome

Loss-of-Function of the Voltage-Gated Sodium Channel NaV1.5 (Channelopathies) in Patients With Irritable Bowel Syndrome

http://www.wikidata.org/entity/Q29544671

about

Inherited arrhythmias: The cardiac channelopathies Disorders of gastrointestinal hypomotility The role of the SCN5A-encoded channelopathy in irritable bowel syndrome and other gastrointestinal disorders Irritable bowel syndrome and diet.Ion channelopathies in functional GI disorders.Stress-induced visceral pain: toward animal models of irritable-bowel syndrome and associated comorbidities.Ranolazine inhibits voltage-gated mechanosensitive sodium channels in human colon circular smooth muscle cells.Expression and function of the Scn5a-encoded voltage-gated sodium channel NaV 1.5 in the rat jejunum.Genetics of irritable bowel syndrome.The virtual intestine: in silico modeling of small intestinal electrophysiology and motility and the applications.The voltage-gated sodium channel NaV 1.9 in visceral pain.Lessons learned--resolving the enigma of genetic factors in IBS.Transit time.Ion channels, ion channel receptors, and visceral hypersensitivity in irritable bowel syndrome.Exploring the genetics of irritable bowel syndrome: a GWA study in the general population and replication in multinational case-control cohorts.Evolution of the Diagnosis of Functional Gut Disorders: Is an Objective Positive Diagnostic Approach Within Reach?Functional variants in the sucrase-isomaltase gene associate with increased risk of irritable bowel syndrome.Early life adversity in piglets induces long-term upregulation of the enteric cholinergic nervous system and heightened, sex-specific secretomotor neuron responses.A GWAS meta-analysis suggests roles for xenobiotic metabolism and ion channel activity in the biology of stool frequency TRPM8 polymorphisms associated with increased risk of IBS-C and IBS-M.Modulation of enteric neurons by interleukin-6 and corticotropin-releasing factor contributes to visceral hypersensitivity and altered colonic motility in a rat model of irritable bowel syndrome.Irritable bowel syndrome and the perinatal period: lower birth weight increases the risk.Voltage-gated sodium channels: (NaV )igating the field to determine their contribution to visceral nociception.Editorial: challenging established perceptions of brain-gut interactions in functional gastrointestinal disorders - brain-gut, gut-brain, or both? Authors' reply.Irritable bowel syndrome (IBS) patients have SCN5A channelopathies that lead to decreased NaV1.5 current and mechanosensitivity.Increased prevalence of rare sucrase-isomaltase (SI) pathogenic variants in irritable bowel syndrome patients.Female-specific Association Between Variants on Chromosome 9 and Self-reported Diagnosis of Irritable Bowel Syndrome.The TPH1 rs211105 gene polymorphism affects abdominal symptoms and quality of life of diarrhea-predominant irritable bowel syndrome.Recent advances in understanding and managing chronic constipation

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P2860

Loss-of-Function of the Voltage-Gated Sodium Channel NaV1.5 (Channelopathies) in Patients With Irritable Bowel Syndrome

http://www.wikidata.org/entity/Q29544671

description

2014 nî lūn-bûn

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2014 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հունիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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P2860

An integrated map of genetic variation from 1,092 human genomes

Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel

The role of genetics in IBS.

Spectrum and prevalence of mutations from the first 2,500 consecutive unrelated patients referred for the FAMILION long QT syndrome genetic test

Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A)

A mutation in telethonin alters Nav1.5 function

Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death

Slowed conduction and ventricular tachycardia after targeted disruption of the cardiac sodium channel gene Scn5a.

Sodium current in human jejunal circular smooth muscle cells.

SCN5A is expressed in human jejunal circular smooth muscle cells.

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