ArticleJournal of lipid research2017
Aromatic residues in the C terminus of apolipoprotein C-III mediate lipid binding and LPL inhibition.
Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed, 26 citations in OpenAlex.
- Apolipoprotein C-III: Risk-factor, Regulator of Triglyceride-rich Lipoprotein Metabolism and Therapeutic Target.Current atherosclerosis reports · 2026Review
- Article
- Effects of emulsifiers on lipid metabolism and performance of yellow-feathered broilers.BMC veterinary research · 2024Article
- Review
- Silencing ApoC3 alleviates LPS-induced acute lung injury by inhibiting TLR signaling pathway.Immunologic research · 2023Article
- The Effect of the Feeding System on Fat Deposition in Yak Subcutaneous Fat.International journal of molecular sciences · 2023Article
- A Tale of Two New Targets for Hypertriglyceridaemia: Which Choice of Therapy?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2022Review
- The Importance of Lipoprotein Lipase Regulation in Atherosclerosis.Biomedicines · 2021Review
- The Roles of ApoC-III on the Metabolism of Triglyceride-Rich Lipoproteins in Humans.Frontiers in endocrinology · 2020Review
- Emerging Evidence that ApoC-III Inhibitors Provide Novel Options to Reduce the Residual CVD.Current atherosclerosis reports · 2019Review
- Association of apolipoprotein C3 with insulin resistance and coronary artery calcium in patients with type 1 diabetes.Journal of clinical lipidologyArticle
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasma apoC-III levels correlate with triglyceride (TG) levels and are a strong predictor of CVD outcomes. ApoC-III elevates TG in part by inhibiting LPL. ApoC-III likely inhibits LPL by competing for lipid binding. To probe this, we used oil-drop tensiometry to characterize binding of six apoC-III variants to lipid/water interfaces. This technique monitors the dependence of lipid binding on surface pressure, which increases during TG hydrolysis by LPL. ApoC-III adsorption increased surface pressure by upward of 18 mN/m at phospholipid/TG/water interfaces. ApoC-III was retained to high pressures at these interfaces, desorbing at 21-25 mN/m. Point mutants, which substituted alanine for aromatic residues, impaired the lipid binding of apoC-III. Adsorption and retention pressures decreased by 1-6 mN/m in point mutants, with the magnitude determined by the location of alanine substitutions. Trp42 was most critical to mediating lipid binding. These results strongly correlate with our previous results, linking apoC-III point mutants to increased LPL binding and activity at lipid surfaces. We propose that aromatic residues in the C-terminal half of apoC-III mediate binding to TG-rich lipoproteins. Increased apoC-III expression in the hypertriglyceridemic state allows apoC-III to accumulate on lipoproteins and inhibit LPL by preventing binding and/or access to substrate.
Indexed as
Identifiers
What Socratic 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 Socratic graph.