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Heart Regeneration in Zebrafish
It is demonstrated histologically that zebrafish fully regenerate hearts within 2 months of 20% ventricular resection, showing that injury-induced cardiomyocyte proliferation in zebra fish can overcome scar formation, allowing cardiac muscle regeneration.
Spectrum of Mutations in Long-QT Syndrome Genes: KVLQT1, HERG, SCN5A, KCNE1, and KCNE2
KVLQT1 and HERG accounted for 87% of identified mutations, and SCN5A, KCNE1, and KCNE2 accounted for the other 13%, and Missense mutations were most common, followed by frameshift mutations, in-frame deletions, and nonsense and splice-site mutations.
Genotype-Phenotype Correlation in the Long-QT Syndrome: Gene-Specific Triggers for Life-Threatening Arrhythmias
Life-threatening arrhythmias in LQTS patients tend to occur under specific circumstances in a gene-specific manner, allowing new insights into the mechanisms that relate the electrophysiological consequences of mutations on specific genes to clinical manifestations and offer the possibility of complementing traditional therapy with gene- specific approaches.
Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias
Genetic factors contribute to the risk of sudden death from cardiac arrhythmias. Here, positional cloning methods establish KVLQT1 as the chromosome 11-linked LQT1 gene responsible for the most
Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel.
K(V)LQT1 is the subunit that coassembles with minK to form I(Ks) channels and I( Ks) dysfunction is a cause of cardiac arrhythmia.