ArticleClinical and experimental nephrology2018
Decreased KLHL3 expression is involved in the pathogenesis of pseudohypoaldosteronism type II caused by cullin 3 mutation in vivo.
Article in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Familial Hyperkalemic Hypertension.Comprehensive Physiology · 2024Review
- Distal convoluted tubule-specific disruption of the COP9 signalosome but not its regulatory target cullin 3 causes tubular injury.American journal of physiology. Renal physiology · 2024Article
- miR-181-5p/KLHL5 Promoted Proliferation and Migration of Gastric Cancer Through Activating METTL3-Mediated m6A Process.Molecular biotechnology · 2024Article
- Insights into the diverse mechanisms and effects of variant CUL3-induced familial hyperkalemic hypertension.Cell communication and signaling : CCS · 2023Review
- Cullin 3 and Blood Pressure Regulation: Insights From Familial Hyperkalemic Hypertension.Hypertension (Dallas, Tex. : 1979) · 2023Review
- Cullin 3 mutant causing familial hyperkalemic hypertension lacks normal activity in the kidney.American journal of physiology. Renal physiology · 2022Article
- Cullin 3 Exon 9 Deletion in Familial Hyperkalemic Hypertension Impairs Cullin3-Ring-E3 Ligase (CRL3) Dynamic Regulation and Cycling.International journal of molecular sciences · 2022Article
- Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice.Pflugers Archiv : European journal of physiology · 2021Article
- Epigenetics of Muscle- and Brain-Specific Expression of KLHL Family Genes.International journal of molecular sciences · 2020Article
- Cullin-3: Renal and Vascular Mechanisms Regulating Blood Pressure.Current hypertension reports · 2020Review
- The WNK signaling pathway and salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Hereditary causes of primary aldosteronism and other disorders of apparent excess mineralocorticoid activity.Gland surgery · 2020Review
- Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding.American journal of physiology. Renal physiology · 2020Review
- Weighted gene co-expression network analysis identified six hub genes associated with rupture of intracranial aneurysms.PloS one · 2020Article
- Cullin-Ring ubiquitin ligases in kidney health and disease.Current opinion in nephrology and hypertension · 2019Review
- Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling Pathway.Journal of the American Society of Nephrology : JASN · 2018Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPseudohypoaldosteronism type II (PHAII) is a hereditary hypertensive disease caused by mutations in four genes: WNK1, WNK4, Kelch-like3 (KLHL3), and cullin3 (CUL3). Recently, it was revealed that CUL3-KLHL3 E3 ligase complex ubiquitinates WNK1 and WNK4, leading to their degradation, and that a common pathogenesis of PHAII is defective WNK degradation due to CUL3-KLHL3 E3 ligase complex impairment. PHAII-causing CUL3 mutations mediate exon9 skipping, producing a CUL3 protein with a 57-amino acid deletion (Δ403-459). However, the pathogenic effects of KLHL3, an adaptor protein that links WNKs with CUL3, in PHAII caused by CUL3 mutation remain unclear.
methodsTo clarify detailed pathophysiological mechanisms underlying PHAII caused by CUL3 mutation in vivo, we generated and analyzed knock-in mice carrying the same CUL3 exon9 deletion (CUL3
resultsCUL3
conclusionKLHL3 expression was decreased in CUL3
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.