ArticleFEBS open bio2023
Inducible over-expression of cardiac Nos1ap causes short QT syndrome in transgenic mice.
Article in FEBS open bio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Genetic Animal Models of Cardiovascular Pathologies.Biomedicines · 2025Review
- Massively parallel reporter assays identify functional enhancer variants at QT interval GWAS loci.bioRxiv : the preprint server for biology · 2025Article
- Interpreting the actionable clinical role of rare variants associated with short QT syndrome.Human genetics · 2024Article
- Cardiac muscle-restricted partial loss of Nos1ap expression has limited but significant impact on electrocardiographic features.G3 (Bethesda, Md.) · 2023Article
- The Physiological Function of nNOS-Associated CAPON Proteins and the Roles of CAPON in Diseases.International journal of molecular sciences · 2023Review
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Authors and funding
10 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence demonstrated that alterations in the QT interval duration on the ECG are not only determined by mutations in genes for ion channels, but also by modulators of ion channels. Changes in the QT interval duration beyond certain thresholds are pathological and can lead to sudden cardiac death. We here focus on the ion channel modulator nitric oxide synthase 1 adaptor protein (Nos1ap). Whole-cell patch-clamp measurements of a conditional transgenic mouse model exhibiting cardiac-specific Nos1ap over-expression revealed a Nos1ap-dependent increase of L-type calcium channel nitrosylation, which led to increased susceptibility to ventricular tachycardias associated with a decrease in QT duration and shortening of APD
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