Associated Papers
Gain-of-function mutations in KCNK3 cause a developmental disorder with sleep apnea.
Sörmann J et al.
Nature Genetics, 2022
Potassium (K+) channels in the pulmonary vasculature: Implications in pulmonary hypertension Physiological, pathophysiological and pharmacological regulation.
Mondéjar-Parreño G et al.
Pharmacology & Therapeutics, 2021
Customized Massive Parallel Sequencing Panel for Diagnosis of Pulmonary Arterial Hypertension.
Castaño JAT et al.
Genes, 2020
33007923 (PubMed )
Supplement: genes-11-01158-s001.zip › genes-941403-supplementary.xlsx › Supplementary_Table_1
Implication of Potassium Channels in the Pathophysiology of Pulmonary Arterial Hypertension.
Le Ribeuz H et al.
Biomolecules, 2020
TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.
Inoue M et al.
Pflugers Archiv : European Journal of Physiology, 2020
Characterization and regulation of wild-type and mutant TASK-1 two pore domain potassium channels indicated in pulmonary arterial hypertension.
Cunningham KP et al.
The Journal of Physiology, 2019
TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications.
Olschewski A et al.
The European Respiratory Journal, 2017
An homozygous mutation in KCNK3 is associated with an aggressive form of hereditary pulmonary arterial hypertension.
Navas Tejedor P et al.
Clinical Genetics, 2017
Molecular Analysis of BMPR2, TBX4, and KCNK3 and Genotype-Phenotype Correlations in Spanish Patients and Families With Idiopathic and Hereditary Pulmonary Arterial Hypertension.
Navas P et al.
Revista Espanola De Cardiologia (english Ed.), 2016
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