ArticleNature communications2016
CCC- and WASH-mediated endosomal sorting of LDLR is required for normal clearance of circulating LDL.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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Who cites it
119 citing papers in PubMed, 228 citations in OpenAlex.
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- Mapping of endosomal proximity proteomes reveals Retromer as a hub for RAB GTPase regulation.Nature communications · 2025Article
- CCDC22 mutations that impair COMMD binding cause attenuated 3C/Ritscher-Schinzel syndrome.BMC medical genomics · 2025Article
- Seasonal and comparative evidence of adaptive gene expression in mammalian brain size plasticity.eLife · 2025Article
- Pathways and Molecular Mechanisms Governing LDL Receptor Regulation.Circulation research · 2025Review
- Mammalian copper homeostasis: physiological roles and molecular mechanisms.Physiological reviews · 2025Review
- Hyperlipidemia-associated specific modules and hub genes revealed by integrative methods of WGCNA and MetaDE.Frontiers in genetics · 2025Article
- Structural basis for Retriever-SNX17 assembly and endosomal sorting.Nature communications · 2024Article
- VPS26 Moonlights as a β-Arrestin-like Adapter for a 7-Transmembrane RGS Protein inBiochemistry · 2024Article
- Assembly and fission of tubular carriers mediating protein sorting in endosomes.Nature reviews. Molecular cell biology · 2024Review
- Genetic variation in CCDC93 is associated with elevated central systolic blood pressure, impaired arterial relaxation, and mitochondrial dysfunction.PLoS genetics · 2024Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 5 countries.
Funding
Abstract
The low-density lipoprotein receptor (LDLR) plays a pivotal role in clearing atherogenic circulating low-density lipoprotein (LDL) cholesterol. Here we show that the COMMD/CCDC22/CCDC93 (CCC) and the Wiskott-Aldrich syndrome protein and SCAR homologue (WASH) complexes are both crucial for endosomal sorting of LDLR and for its function. We find that patients with X-linked intellectual disability caused by mutations in CCDC22 are hypercholesterolaemic, and that COMMD1-deficient dogs and liver-specific Commd1 knockout mice have elevated plasma LDL cholesterol levels. Furthermore, Commd1 depletion results in mislocalization of LDLR, accompanied by decreased LDL uptake. Increased total plasma cholesterol levels are also seen in hepatic COMMD9-deficient mice. Inactivation of the CCC-associated WASH complex causes LDLR mislocalization, increased lysosomal degradation of LDLR and impaired LDL uptake. Furthermore, a mutation in the WASH component KIAA0196 (strumpellin) is associated with hypercholesterolaemia in humans. Altogether, this study provides valuable insights into the mechanisms regulating cholesterol homeostasis and LDLR trafficking.
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Registered trials
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