Associated Papers
MOG1L18F-mediated increase in late sodium current produces Long QT Syndrome.
Socuéllamos PG et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
Molecular mechanism for the interaction of MOG1 with the intracellular loop II of cardiac sodium channel Nav1.5 and its role in arrhythmias.
Bai X et al.
Journal of Molecular and Cellular Cardiology, 2025
1029 genomes of self-declared healthy individuals from India reveal prevalent and clinically relevant cardiac ion channelopathy variants.
Bajaj A et al.
Human Genomics, 2022
Atrial fibrillation-a complex polygenetic disease.
Andersen JH et al.
European Journal of Human Genetics : Ejhg, 2021
Genetic interpretation and clinical translation of minor genes related to Brugada syndrome.
Campuzano O et al.
Human Mutation, 2019
Morphogenetic defects underlie Superior Coloboma, a newly identified closure disorder of the dorsal eye.
Hocking JC et al.
Plos Genetics, 2018
Impact of Ancestral Differences and Reassessment of the Classification of Previously Reported Pathogenic Variants in Patients With Brugada Syndrome in the Genomic Era: A SADS-TW BrS Registry.
Chen CJ et al.
Frontiers in Genetics, 2018
Ion channelopathies associated genetic variants as the culprit for sudden unexplained death.
Wang S et al.
Forensic Science International, 2017
Rare variants in genes encoding the cardiac sodium channel and associated compounds and their impact on outcome of catheter ablation of atrial fibrillation.
Husser D et al.
Plos One, 2017
Brugada syndrome: a fatal disease with complex genetic etiologies - still a long way to go.
Wu Y et al.
Forensic Sciences Research, 2017
Post-mortem whole-exome sequencing (WES) with a focus on cardiac disease-associated genes in five young sudden unexplained death (SUD) cases.
Neubauer J et al.
International Journal of Legal Medicine, 2016
Diagnostic yield of molecular autopsy in patients with sudden arrhythmic death syndrome using targeted exome sequencing.
Nunn LM et al.
Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology, 2016
Cardiac Sodium Channel Mutations: Why so Many Phenotypes?
Liu M et al.
Current Topics in Membranes, 2016
Comprehensive Genetic Characterization of a Spanish Brugada Syndrome Cohort.
Selga E et al.
Plos One, 2015
Diseases caused by mutations in Nav1.5 interacting proteins.
Kyle JW et al.
Cardiac Electrophysiology Clinics, 2014
Brugada syndrome risk loci seem protective against atrial fibrillation.
Andreasen L et al.
European Journal of Human Genetics : Ejhg, 2014
Cardiac sodium channel mutations: why so many phenotypes?
Liu M et al.
Nature Reviews. Cardiology, 2014
Integrated analysis of germline and somatic variants in ovarian cancer.
Kanchi KL et al.
Nature Communications, 2014
Identifying potential functional impact of mutations and polymorphisms: linking heart failure, increased risk of arrhythmias and sudden cardiac death.
Jagu B et al.
Frontiers in Physiology, 2013
Arrhythmogenesis in Brugada syndrome: impact and constrains of current concepts.
Bébarová M
International Journal of Cardiology, 2013
The genetic component of Brugada syndrome.
Nielsen MW et al.
Frontiers in Physiology, 2013
A novel nonsense variant in Nav1.5 cofactor MOG1 eliminates its sodium current increasing effect and may increase the risk of arrhythmias.
Olesen MS et al.
The Canadian Journal of Cardiology, 0
Patient-derived glioblastoma organoids reflect tumor heterogeneity and treatment sensitivity.
Verduin M et al.
Neuro-oncology Advances, 0