Associated Papers
Familial Hyperkalemic Hypertension.
Cornelius RJ et al.
Comprehensive Physiology, 2024
Aldosterone defects in infants and young children with hyperkalemia: A single center retrospective study.
Liu X et al.
Frontiers in Pediatrics, 2023
A case report of pseudohypoaldosteronism type II with a homozygous KLHL3 variant accompanied by hyperthyroidism.
Zhang R et al.
Bmc Endocrine Disorders, 2021
Hypertension Accompanied by Hyperaldosteronism, Hyperkalemia, and Hyperchloremic Acidosis: A Case Report and Literature Review.
Yang Y et al.
Case Reports in Endocrinology, 2020
Systematic analysis of the intersection of disease mutations with protein modifications.
Simpson CM et al.
Bmc Medical Genomics, 2019
31345222 (PubMed )
Supplement: 12920_2019_543_MOESM5_ESM.xlsx › S4
Unveiling the Distinct Mechanisms by which Disease-Causing Mutations in the Kelch Domain of KLHL3 Disrupt the Interaction with the Acidic Motif of WNK4 through Molecular Dynamics Simulation.
Wang L et al.
Biochemistry, 2019
30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Mineralocorticoid receptor and NaCl transport mechanisms in the renal distal nephron.
Shibata S
The Journal of Endocrinology, 2017
Phosphorylation of KLHL3 at serine 433 impairs its interaction with the acidic motif of WNK4: a molecular dynamics study.
Wang L et al.
Protein Science : a Publication of the Protein Society, 2017
Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3.
Ishizawa K et al.
Biochemical and Biophysical Research Communications, 2016
Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation.
Shibata S et al.
Proceedings of the National Academy of Sciences of the United States of America, 2014
Structural and biochemical characterization of the KLHL3-WNK kinase interaction important in blood pressure regulation.
Schumacher FR et al.
The Biochemical Journal, 2014
Detection of mutations in KLHL3 and CUL3 in families with FHHt (familial hyperkalaemic hypertension or Gordon's syndrome).
Glover M et al.
Clinical Science (london, England : 1979), 2014
The CUL3-KLHL3 E3 ligase complex mutated in Gordon's hypertension syndrome interacts with and ubiquitylates WNK isoforms: disease-causing mutations in KLHL3 and WNK4 disrupt interaction.
Ohta A et al.
The Biochemical Journal, 2013
Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities.
Boyden LM et al.
Nature, 2012
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