ArticleAmerican journal of physiology. Renal physiology2018
Dual gain and loss of cullin 3 function mediates familial hyperkalemic hypertension.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK.The Journal of physiology · 2025Article
- Cullin-3 regulates the renal baroreceptor machinery that controls renin gene expression.JCI insight · 2025Article
- 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
- 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
- COP9 signalosome deletion promotes renal injury and distal convoluted tubule remodeling.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
- NovelHypertension (Dallas, Tex. : 1979) · 2022Article
- Comorbidities Caused by a Corrupt Cullin 3: Lessons Learned From Bedside to Bench.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Downregulation of Cullin 3 Ligase Signaling Pathways Contributes to Hypertension in Preeclampsia.Frontiers in cardiovascular medicine · 2021Article
- 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
- Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding.American journal of physiology. Renal physiology · 2020Review
- Cullin-Ring ubiquitin ligases in kidney health and disease.Current opinion in nephrology and hypertension · 2019Review
- Conditional deletion of smooth muscle Cullin-3 causes severe progressive hypertension.JCI insight · 2019Article
- 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
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Familial hyperkalemic hypertension is caused by mutations in with-no-lysine kinases (WNKs) or in proteins that mediate their degradation, kelch-like 3 (KLHL3) and cullin 3 (CUL3). Although the mechanisms by which WNK and KLHL3 mutations cause the disease are now clear, the effects of the disease-causing CUL3Δ403-459 mutation remain controversial. Possible mechanisms, including hyperneddylation, altered ubiquitin ligase activity, decreased association with the COP9 signalosome (CSN), and increased association with and degradation of KLHL3 have all been postulated. Here, we systematically evaluated the effects of Cul3Δ403-459 using cultured kidney cells. We first identified that the catalytically active CSN subunit jun activation domain-binding protein-1 (JAB1) does not associate with the deleted Cul3 4-helix bundle domain but instead with the adjacent α/β
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