Associated Papers
A case report of Graves' disease combined with pseudohypoaldosteronism type IID in a child.
Yao J et al.
Translational Pediatrics, 2025
The evolving concepts of KS-WNK1 effect on NCC activity.
Chávez-Canales M et al.
American Journal of Physiology. Renal Physiology, 2025
Familial Hyperkalemic Hypertension.
Cornelius RJ et al.
Comprehensive Physiology, 2024
Pseudohypoaldosteronism type II and sensory neuropathy associated with a heterozygous pathogenic variant in KLHL3 gene, a case report.
Davion JB et al.
Heliyon, 2024
Insights into the diverse mechanisms and effects of variant CUL3-induced familial hyperkalemic hypertension.
Sharma P et al.
Cell Communication and Signaling : Ccs, 2023
Identification of a novel KLHL3-interacting motif in the C-terminal region of WNK4.
Wang L et al.
Biochemical and Biophysical Research Communications, 2023
Aldosterone defects in infants and young children with hyperkalemia: A single center retrospective study.
Liu X et al.
Frontiers in Pediatrics, 2023
Multiple molecular mechanisms are involved in the activation of the kidney sodium-chloride cotransporter by hypokalemia.
Murillo-de-Ozores AR et al.
Kidney International, 2022
The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.
Lin SC et al.
Biomedicines, 2022
Generation and analysis of pseudohypoaldosteronism type II knock-in mice caused by a nonsense KLHL3 mutation in the Kelch domain.
Lin CM et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2022
Sequence and structural variations determining the recruitment of WNK kinases to the KLHL3 E3 ligase.
Chen Z et al.
The Biochemical Journal, 2022
A case report of pseudohypoaldosteronism type II with a homozygous KLHL3 variant accompanied by hyperthyroidism.
Zhang R et al.
Bmc Endocrine Disorders, 2021
Role of KLHL3 and dietary K+ in regulating KS-WNK1 expression.
Ostrosky-Frid M et al.
American Journal of Physiology. Renal Physiology, 2021
WNK4 kinase: from structure to physiology.
Murillo-de-Ozores AR et al.
American Journal of Physiology. Renal Physiology, 2021
Mutation affecting the conserved acidic WNK1 motif causes inherited hyperkalemic hyperchloremic acidosis.
Louis-Dit-Picard H et al.
The Journal of Clinical Investigation, 2020
The WNK signaling pathway and salt-sensitive hypertension.
Furusho T et al.
Hypertension Research : Official Journal of the Japanese Society of Hypertension, 2020
Hypertension Accompanied by Hyperaldosteronism, Hyperkalemia, and Hyperchloremic Acidosis: A Case Report and Literature Review.
Yang Y et al.
Case Reports in Endocrinology, 2020
Physiological Processes Modulated by the Chloride-Sensitive WNK-SPAK/OSR1 Kinase Signaling Pathway and the Cation-Coupled Chloride Cotransporters.
Murillo-de-Ozores AR et al.
Frontiers in Physiology, 2020
Kelch-like proteins: Physiological functions and relationships with diseases.
Shi X et al.
Pharmacological Research, 2019
Learning Physiology From Inherited Kidney Disorders.
van der Wijst J et al.
Physiological Reviews, 2019
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
Generation and analysis of a mouse model of pseudohypoaldosteronism type II caused by KLHL3 mutation in BTB domain.
Lin CM et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2019
The role of ubiquitination and deubiquitination in the regulation of cell junctions.
Cai J et al.
Protein & Cell, 2018
WNK4 is indispensable for the pathogenesis of pseudohypoaldosteronism type II caused by mutant KLHL3.
Susa K et al.
Biochemical and Biophysical Research Communications, 2017
WNK signalling pathways in blood pressure regulation.
Murthy M et al.
Cellular and Molecular Life Sciences : Cmls, 2017
Familial Hyperkalemia and Hypertension (FHHt) and KLHL3: Description of a Family with a New Recessive Mutation (S553L) Compared to a Family with a Dominant Mutation, Q309R, with Analysis of Urinary Sodium Chloride Cotransporter.
Kliuk-Ben Bassat O et al.
Nephron, 2017
Hyperkalemia in young children: blood pressure checked?
Hollander R et al.
European Journal of Pediatrics, 2016
Kelch-like 3/Cullin 3 ubiquitin ligase complex and WNK signaling in salt-sensitive hypertension and electrolyte disorder.
Sohara E et al.
Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 2016
Paracellular transport in the collecting duct.
Hou J
Current Opinion in Nephrology and Hypertension, 2016
Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension.
Zhang C et al.
Biochemical and Biophysical Research Communications, 2016
Involvement of selective autophagy mediated by p62/SQSTM1 in KLHL3-dependent WNK4 degradation.
Mori Y et al.
The Biochemical Journal, 2015
Impaired degradation of WNK by Akt and PKA phosphorylation of KLHL3.
Yoshizaki Y et al.
Biochemical and Biophysical Research Communications, 2015
Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia.
Schumacher FR et al.
Embo Molecular Medicine, 2015
Critical role of the SPAK protein kinase CCT domain in controlling blood pressure.
Zhang J et al.
Human Molecular Genetics, 2015
Hypercalciuria in familial hyperkalemia and hypertension with KLHL3 mutations.
Mayan H et al.
Nephron, 2015
Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3.
McCormick JA et al.
The Journal of Clinical Investigation, 2014
Impaired degradation of WNK1 and WNK4 kinases causes PHAII in mutant KLHL3 knock-in mice.
Susa K et al.
Human Molecular Genetics, 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
Decrease of WNK4 ubiquitination by disease-causing mutations of KLHL3 through different molecular mechanisms.
Mori Y et al.
Biochemical and Biophysical Research Communications, 2013
Kelch-like 3 and Cullin 3 regulate electrolyte homeostasis via ubiquitination and degradation of WNK4.
Shibata S et al.
Proceedings of the National Academy of Sciences of the United States of America, 2013
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
Impaired KLHL3-mediated ubiquitination of WNK4 causes human hypertension.
Wakabayashi M et al.
Cell Reports, 2013
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron.
Louis-Dit-Picard H et al.
Nature Genetics, 2012
Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities.
Boyden LM et al.
Nature, 2012
[KLHL3 and CULLIN-3: new genes involved in familial hypertension].
Louis-Dit-Picard H et al.
Medecine Sciences : M/s, 0