ArticleChannels (Austin, Tex.)2020
The mutation L69P in the PAS domain of the hERG potassium channel results in LQTS by trafficking deficiency.
Article in Channels (Austin, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Functional characterization and allele-specific RNA interference-based rescue of KCNH2 p.F68C variant associated with long QT syndrome.Molecular genetics and genomics : MGG · 2026Article
- Opioids-Induced Long QT Syndrome: A Challenge to Cardiac Health.Cardiovascular toxicology · 2024Review
- Role and mechanism of chaperones calreticulin and ERP57 in restoring trafficking to mutant HERG‑A561V protein.International journal of molecular medicine · 2021Article
- Computational analysis of long QT syndrome type 2 and the therapeutic effects of KCNQ1 antibodies.Digital healthArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
The congenital long QT syndrome (LQTS) is a cardiac disorder characterized by a prolonged QT interval on the electrocardiogram and an increased susceptibility to ventricular arrhythmias and sudden cardiac death. A frequent cause for LQTS is mutations in the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.