ArticleFEBS letters2013
Disease-causing mutations in KLHL3 impair its effect on WNK4 degradation.
Article in FEBS letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Sustained Transcriptional Response to Lipopolysaccharide and Interleukin-4 in an Immortalized Mouse Microglial Cell Line.Molecular neurobiology · 2026Article
- Familial Hyperkalemic Hypertension.Comprehensive Physiology · 2024Review
- KLHL3-dependent WNK4 degradation affected by potassium through the neddylation and autophagy pathway.BMC nephrology · 2023Article
- The serine-threonine protein phosphatases that regulate the thiazide-sensitive NaCl cotransporter.Frontiers in physiology · 2023Review
- UBR5 is a novel regulator of WNK1 stability.American journal of physiology. Cell physiology · 2022Article
- A narrative review of Hyporeninemic hypertension-an indicator for monogenic forms of hypertension.Pediatric medicine (Hong Kong, China) · 2022Article
- Roles of Cullin-RING Ubiquitin Ligases in Cardiovascular Diseases.Biomolecules · 2022Review
- Aldosterone-Regulated Sodium Transport and Blood Pressure.Frontiers in physiology · 2022Review
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- Regulatory control of the Na-Cl co-transporter NCC and its therapeutic potential for hypertension.Acta pharmaceutica Sinica. B · 2021Review
- High glucose-induced effects on NaAmerican journal of physiology. Cell physiology · 2021Article
- Mutation affecting the conserved acidic WNK1 motif causes inherited hyperkalemic hyperchloremic acidosis.The Journal of clinical investigation · 2020Article
- The WNK signaling pathway and salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Role of the Ubiquitin Proteasome System in the Regulation of Blood Pressure: A Review.International journal of molecular sciences · 2020Review
- Genome Resequencing Reveals Congenital Causes of Embryo and Nestling Death in Crested Ibis (Nipponia nippon).Genome biology and evolution · 2019Article
- Severe Arterial Hypertension from Cullin 3 Mutations Is Caused by Both Renal and Vascular Effects.Journal of the American Society of Nephrology : JASN · 2019Article
- Article
- Decreased KLHL3 expression is involved in the pathogenesis of pseudohypoaldosteronism type II caused by cullin 3 mutation in vivo.Clinical and experimental nephrology · 2018Article
- Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling Pathway.Journal of the American Society of Nephrology : JASN · 2018Article
- Dual gain and loss of cullin 3 function mediates familial hyperkalemic hypertension.American journal of physiology. Renal physiology · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Mutations in with-no-lysine (K) kinase 4 (WNK4) and a ubiquitin E3 ligase complex component kelch-like 3 (KLHL3) both cause pseudohypoaldosteronism II (PHAII), a hereditary form of hypertension. We determined whether WNK4 or its effector is regulated by KLHL3 in Xenopus oocytes. KLHL3 inhibited the positive effect of WNK4 on Na(+)-Cl(-) cotransporter (NCC) by decreasing WNK4 protein abundance without decreasing that of NCC and the downstream kinase OSR1 directly. Ubiquitination and degradation of WNK4 were induced by KLHL3. The effect of KLHL3 on WNK4 degradation was blocked by a dominant negative form of cullin 3. All five PHAII mutations of KLHL3 tested disrupted the regulation on WNK4. We conclude that KLHL3 is a substrate adaptor for WNK4 in a ubiquitin E3 ligase complex.
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