ArticleJournal of the American Heart Association2017
The Impact of Heterozygous
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Equivalent gain-of-function variants in KCNK3 and KCNK9 and their contribution to distinct TASK K2P channelopathies.The Journal of general physiology · 2026Article
- Early Detection and Therapy of Asymptomatic Group 1 Pulmonary Hypertension Following Genetic Testing: A Case Involving FamilialCJC open · 2026Article
- N-Substituted-2-(9H-Xanthen-9-yl)acetamide Derivatives Induce In Vitro Colon Cancer Cell Death via TASK-1 Inhibition: Lead Compounds for Further Optimization as TASK-1-Targeted Therapeutics in Colorectal Cancer.International journal of molecular sciences · 2026Article
- Article
- KPharmaceuticals (Basel, Switzerland) · 2026Review
- Gene-based association study reveals a distinct female genetic signal in primary hypertension.Human genetics · 2023Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Gain-of-function mutations in KCNK3 cause a developmental disorder with sleep apnea.Nature genetics · 2022Article
- Review
- Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022Review
- Ion channels as convergence points in the pathology of pulmonary arterial hypertension.Biochemical Society transactions · 2021Review
- KCNK3 Mutation Causes Altered Immune Function in Pulmonary Arterial Hypertension Patients and Mouse Models.International journal of molecular sciences · 2021Article
- 'There and Back Again'-Forward Genetics and Reverse Phenotyping in Pulmonary Arterial Hypertension.Genes · 2020Review
- Implication of Potassium Channels in the Pathophysiology of Pulmonary Arterial Hypertension.Biomolecules · 2020Review
- TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.Pflugers Archiv : European journal of physiology · 2020Review
- The role of genomics and genetics in pulmonary arterial hypertension.Global cardiology science & practice · 2020Review
- Molecular genetic framework underlying pulmonary arterial hypertension.Nature reviews. Cardiology · 2020Review
- Article
- Characterization and regulation of wild-type and mutant TASK-1 two pore domain potassium channels indicated in pulmonary arterial hypertension.The Journal of physiology · 2019Article
- Twik-2Physiological reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHeterozygous loss of function mutations in the METHODS AND
resultsWe engineered homomeric and heterodimeric mutant and nonmutant KCNK3 channels associated with PAH. Using whole-cell patch-clamp electrophysiology in human pulmonary artery smooth muscle and COS7 cell lines, we determined that homomeric and heterodimeric mutant channels in heterozygous KCNK3 conditions lead to mutation-specific severity of channel dysfunction. Both wildtype and mutant KCNK3 channels were activated by ONO-RS-082 (10 μmol/L), causing cell hyperpolarization. We observed robust gene expression of
conclusionsHeterozygous
Indexed as
Identifiers
What OpenQuestion holds
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.