Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation
Author:
Funder
NHLBI
NIGMS
Publisher
American Society for Clinical Investigation
Subject
General Medicine
Link
https://insight.jci.org/articles/view/152050/files/pdf
Reference66 articles.
1. Voltage-Gated Sodium Channel β1/β1B Subunits Regulate Cardiac Physiology and Pathophysiology
2. Sodium Channel β Subunits: Emerging Targets in Channelopathies
3. Confirming the recessive inheritance of SCN1B mutations in developmental epileptic encephalopathy
4. SCN1B‐linked early infantile developmental and epileptic encephalopathy
5. A Functional Null Mutation of SCN1B in a Patient with Dravet Syndrome
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1. Decreased ability to manage increases in reactive oxygen species may underlie susceptibility to arrhythmias in mice lacking Scn1b;American Journal of Physiology-Heart and Circulatory Physiology;2024-10-01
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3. Sinus node dysfunction and atrial fibrillation—Relationships, clinical phenotypes, new mechanisms, and treatment approaches;Ageing Research Reviews;2023-04
4. Ranolazine exerts atrial antiarrhythmic effects in a rat model of monocrotaline‐induced pulmonary hypertension;Basic & Clinical Pharmacology & Toxicology;2023-03
5. Epilepsy and sudden unexpected death in epilepsy in a mouse model of human SCN1B-linked developmental and epileptic encephalopathy;Brain Communications;2023
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