ArticleJournal of lipid research2013
S-nitrosylation of ARH is required for LDL uptake by the LDL receptor.
Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- S-Nitrosylation: Mechanistic Links between Nitric Oxide Signaling and Atherosclerosis.Current atherosclerosis reports · 2025Review
- Clinical associations and potential cellular mechanisms linking G6PD deficiency and atherosclerotic cardiovascular disease.npj metabolic health and disease · 2025Review
- Biomechanics-mediated endocytosis in atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Targeting protein modifications in metabolic diseases: molecular mechanisms and targeted therapies.Signal transduction and targeted therapy · 2023Review
- A multienzyme S-nitrosylation cascade regulates cholesterol homeostasis.Cell reports · 2022Article
- Relationship between Brain Metabolic Disorders and Cognitive Impairment: LDL Receptor Defect.International journal of molecular sciences · 2022Review
- Endocytosis in the adaptation to cellular stress.Cell stress · 2020Review
- Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol.Journal of lipid research · 2016Article
- Reciprocal regulation of endocytosis and metabolism.Cold Spring Harbor perspectives in biology · 2014Review
- The LRP6 rs2302685 polymorphism is associated with increased risk of myocardial infarction.Lipids in health and disease · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The LDL receptor (LDLR) relies upon endocytic adaptor proteins for internalization of lipoproteins. The results of this study show that the LDLR adaptor autosomal recessive hypercholesterolemia protein (ARH) requires nitric oxide to support LDL uptake. Nitric oxide nitrosylates ARH at C199 and C286, and these posttranslational modifications are necessary for association of ARH with the adaptor protein 2 (AP-2) component of clathrin-coated pits. In the absence of nitrosylation, ARH is unable to target LDL-LDLR complexes to coated pits, resulting in poor LDL uptake. The role of nitric oxide on LDLR function is specific for ARH because inhibition of nitric oxide synthase activity impairs ARH-supported LDL uptake but has no effect on other LDLR-dependent lipoprotein uptake processes, including VLDL remnant uptake and dab2-supported LDL uptake. These findings suggest that cells that depend upon ARH for LDL uptake can control which lipoproteins are internalized by their LDLRs through changes in nitric oxide.
Indexed as
Identifiers
What OpenQuestion holds
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.