Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Dual gain and loss of cullin 3 function mediates familial hyperkalemic hypertension.

American journal of physiology. Renal physiology - 1 Oct 2018

Cornelius Ryan J, Zhang Chong, Erspamer Kayla J, Agbor Larry N, Sigmund Curt D, Singer Jeffrey D, Yang Chao-Ling, Ellison David H

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adaptor Proteins, Signal Transducing
Share to COP9 Signalosome Complex

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cullin Proteins

Share to Hypertension

Share to Kidney

Share to Microfilament Proteins

Share to Minor Histocompatibility Antigens

Share to Ubiquitination

Source

Open in PubMed Open full text

Identifiers

PMID: 29897280
DOI: 10.1152/ajprenal.00602.2017
PMCID: PMC6230741

Genes

KLHL3
WNK4
CUL3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dual gain and loss of cullin 3 function mediates familial hyperkalemic hypertension.PMID 29897280Read ↗

Hypertension-causing cullin 3 mutations disrupt COP9 signalosome binding.Semantic proximity Read ↗

Renal effects of cullin 3 mutations causing familial hyperkalemic hypertension.Semantic proximity Read ↗

Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects.Semantic proximity Read ↗

Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia.Semantic proximity Read ↗

Kelch-like 3 and Cullin 3 regulate electrolyte homeostasis via ubiquitination and degradation of WNK4.Semantic proximity Read ↗

Cullin 3 Exon 9 Deletion in Familial Hyperkalemic Hypertension Impairs Cullin3-Ring-E3 Ligase (CRL3) Dynamic Regulation and CyclingSemantic proximity Read ↗

Decreased KLHL3 expression is involved in the pathogenesis of pseudohypoaldosteronism type II caused by cullin 3 mutation in vivo.Semantic proximity Read ↗

Mutation affecting the conserved acidic WNK1 motif causes inherited hyperkalemic hyperchloremic acidosis.Semantic proximity Read ↗

Impaired degradation of WNK1 and WNK4 kinases causes PHAII in mutant KLHL3 knock-in mice.Semantic proximity Read ↗

Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities.Semantic proximity Read ↗

Mechanisms and controversies in mutant Cul3-mediated familial hyperkalemic hypertension.Semantic proximity Read ↗

Role of KLHL3 and dietary K+ in regulating KS-WNK1 expression.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.