ArticleJournal of lipid research2016
Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol.
Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Dissecting genetic regulation of metabolic coordination.Briefings in bioinformatics · 2025Article
- dab2 is required for the scavenging function of lymphatic endothelial cells in the zebrafish meninges.Scientific reports · 2024Article
- Article
- Mechanism of the Regulation of Plasma Cholesterol Levels by PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Relationship between Brain Metabolic Disorders and Cognitive Impairment: LDL Receptor Defect.International journal of molecular sciences · 2022Review
- Transcriptome Profile Reveals Genetic and Metabolic Mechanisms Related to Essential Fatty Acid Content of IntramuscularMetabolites · 2022Article
- Endocytosis in the context-dependent regulation of individual and collective cell properties.Nature reviews. Molecular cell biology · 2021Review
- A human cell atlas of fetal gene expression.Science (New York, N.Y.) · 2020Article
- Dab2 gene variant is associated with increased coronary artery disease risk in Chinese Han population.Medicine · 2020Article
- Cholesterol uptake and efflux are impaired in human trophoblast cells from pregnancies with maternal supraphysiological hypercholesterolemia.Scientific reports · 2020Article
- Endocytic Adaptors in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020Review
- Endocytic Adaptor Proteins in Health and Disease: Lessons from Model Organisms and Human Mutations.Cells · 2019Review
- HDAC9 Polymorphism Alters Blood Gene Expression in Patients with Large Vessel Atherosclerotic Stroke.Translational stroke research · 2019Article
- Deficiency of Dab2 (Disabled Homolog 2) in Myeloid Cells Exacerbates Inflammation in Liver and Atherosclerotic Plaques in LDLR (Low-Density Lipoprotein Receptor)-Null Mice-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- News on the molecular regulation and function of hepatic low-density lipoprotein receptor and LDLR-related protein 1.Current opinion in lipidology · 2017Review
- Disabled-2 Determines Commitment of a Pre-adipocyte Population in Juvenile Mice.Scientific reports · 2016Article
- Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice.Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
High serum cholesterol (hypercholesterolemia) strongly associates with cardiovascular diseases as the atherogenic LDLs promote atheroma development in arteries (atherosclerosis). LDL clearance from the circulation by LDL receptor (LDLR)-mediated endocytosis by hepatic and peripheral tissues and subsequent feedback regulation of endogenous synthesis of cholesterol is a key determinant of serum LDL level. Human mutation analysis revealed that autosomal recessive hypercholesterolemia (ARH), an LDLR endocytic adaptor, perturbs LDLR function and thus impacts serum cholesterol levels. In our genetic analysis of mutant mice, we found that deletion of another LDLR endocytic adaptor, Disabled-2 (Dab2), only slightly affected serum cholesterol levels. However, elimination of both arh and dab2 genes in mice resulted in profound hypercholesterolemia similar to that resulting from ldlr homozygous deletion. In the liver, Dab2 is expressed in sinusoid endothelial cells but not in hepatocytes. When deleting both Dab2 and Arh, HMG-CoA reductase level increased to the level similar to that of ldlr knockout. Thus, in the absence of Arh, Dab2 in liver endothelial cells regulates cholesterol synthesis in hepatocytes. We conclude that the combination of Arh and Dab2 is responsible for the majority of adaptor function in LDLR endocytosis and LDLR-mediated cholesterol homeostasis.
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Registered trials
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.