Anonymous (2026). In vivo analysis of trafficking and functional impact of hERG pore-domain missense variants in a CRISPR/Cas9-engineered C. elegans model of long QT syndrome.. Heart rhythm.
Anonymous. In vivo analysis of trafficking and functional impact of hERG pore-domain missense variants in a CRISPR/Cas9-engineered C. elegans model of long QT syndrome.. Heart rhythm. 2026; PMID: 42190933
Anonymous. In vivo analysis of trafficking and functional impact of hERG pore-domain missense variants in a CRISPR/Cas9-engineered C. elegans model of long QT syndrome.[J]. Heart rhythm. 2026.
@article{paper2026,
author = {Anonymous},
title = {In vivo analysis of trafficking and functional impact of hERG pore-domain missense variants in a CRISPR/Cas9-engineered C. elegans model of long QT syndrome.},
journal = {Heart rhythm},
year = {2026},
note = {PMID: 42190933},
}
TY - JOUR AU - Anonymous TI - In vivo analysis of trafficking and functional impact of hERG pore-domain missense variants in a CRISPR/Cas9-engineered C. elegans model of long QT syndrome. T2 - Heart rhythm PY - 2026 AN - PMID:42190933 ER -
Loss-of-function variants in KCNH2, which encodes hERG, are responsible for long QT syndrome type 2 (LQT2), a major cause of sudden cardiac death. Most hERG pore-domain missense variants are associated with severe LQT2. However, functional heterogeneity exists among these variants, with a small subset associated with milder phenotypes. Only a limited number of these atypical variants have been functionally characterized. Caenorhabditis elegans expresses UNC-103, a voltage-gated K