Associated Papers
Pseudohypoaldosteronism type 1b in fraternal twins of a Chinese family: report of two cases and literature review.
Gao Z et al.
Archives of Endocrinology and Metabolism, 2023
Neonatal presentation of a patient with Liddle syndrome, South Africa.
Steyn N et al.
African Journal of Laboratory Medicine, 2023
Kidney ion handling genes and their interaction in blood pressure control.
An C et al.
Bioscience Reports, 2022
Rare Variants in Genes Encoding Subunits of the Epithelial Na+ Channel Are Associated With Blood Pressure and Kidney Function.
Blobner BM et al.
Hypertension (dallas, Tex. : 1979), 2022
Human epithelial Na+ channel missense variants identified in the GenSalt study alter channel activity.
Ray EC et al.
American Journal of Physiology. Renal Physiology, 2016
Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases.
Hanukoglu I et al.
Gene, 2016
Assessment of epithelial sodium channel variants in nonwhite cystic fibrosis patients with non-diagnostic CFTR genotypes.
Brennan ML et al.
Journal of Cystic Fibrosis : Official Journal of the European Cystic Fibrosis Society, 2016
Mutations in the amiloride-sensitive epithelial sodium channel in patients with cystic fibrosis-like disease.
Azad AK et al.
Human Mutation, 2009
Lack of association of functional variants in alpha-ENaC gene and essential hypertension in two ethnic groups in China.
Wang XF et al.
Kidney & Blood Pressure Research, 2008
The epithelial sodium channel in hypertension: genetic heterogeneity and implications for treatment with amiloride.
Swift PA et al.
American Journal of Pharmacogenomics : Genomics-related Research in Drug Development and Clinical Practice, 2004
Epithelial sodium channel, salt intake, and hypertension.
Hummler E
Current Hypertension Reports, 2003
Association of a sodium channel alpha subunit promoter variant with blood pressure.
Iwai N et al.
Journal of the American Society of Nephrology : Jasn, 2002
Genome Analysis of Osteosarcoma Progression Samples Identifies FGFR1 Overexpression as a Potential Treatment Target and CHM as a Candidate Tumor Suppressor Gene.
Barøy T et al.
Plos One, 0