ArticleFrontiers in cardiovascular medicine2025
Pathogenic KCNH2-G53S variant in the PAS domain influences the electrophysiological phenotype in long QT syndrome type 2.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Personalized in vitro models reveal functional impact of aHeart rhythm O2 · 2026Article
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7 authors.
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Abstract
Background: Long QT syndrome type 2 (LQT2) is an arrythmia caused by loss-of-function mutations in KCNH2, leading to impaired Kv11.1 channel function. Objective: To better understand LQT2, we examined the electrophysiological differences related to the G53S variant, which is located within the PAS domain of KCNH2, using patient-specific human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (hiPSC-CMs). Methods: We generated hiPSC-CMs from a patient harboring the KCNH2 Results: The patient harboring KCNH2 Conclusion: Our analysis of hiPSC-CMs carrying a heterozygous KCNH2
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