ArticleJournal of lipid research2010
Functional analysis of the missense APOC3 mutation Ala23Thr associated with human hypotriglyceridemia.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Associations of the APOC3 rs5128 polymorphism with plasma APOC3 and lipid levels: a meta-analysis.Lipids in health and disease · 2015Pooled it
- Article
- Article
- Identity-by-Descent Mapping Identifies Major Locus for Serum Triglycerides in Amerindians Largely Explained by anCirculation. Cardiovascular genetics · 2017Article
- The apolipoprotein C-III (Gln38Lys) variant associated with human hypertriglyceridemia is a gain-of-function mutation.Journal of lipid research · 2017Article
- A human APOC3 missense variant and monoclonal antibody accelerate apoC-III clearance and lower triglyceride-rich lipoprotein levels.Nature medicine · 2017Article
- A Novel Role for RARα Agonists as Apolipoprotein CIII Inhibitors Identified from High Throughput Screening.Scientific reports · 2017Article
- Aromatic residues in the C terminus of apolipoprotein C-III mediate lipid binding and LPL inhibition.Journal of lipid research · 2017Article
- APOC3 Protein Is Not a Predisposing Factor for Fat-induced Nonalcoholic Fatty Liver Disease in Mice.The Journal of biological chemistry · 2017Article
- Targeting ApoC-III to Reduce Coronary Disease Risk.Current atherosclerosis reports · 2016Review
- Metabolic Characterization of a Rare Genetic Variation Within APOC3 and Its Lipoprotein Lipase-Independent Effects.Circulation. Cardiovascular genetics · 2016Article
- Sugar consumption, metabolic disease and obesity: The state of the controversy.Critical reviews in clinical laboratory sciences · 2016Review
- Apolipoprotein C-III: a potent modulator of hypertriglyceridemia and cardiovascular disease.Current opinion in endocrinology, diabetes, and obesity · 2015Review
- Loss-of-function mutations in APOC3, triglycerides, and coronary disease.The New England journal of medicine · 2014Article
- Overexpression of apolipoprotein C-III decreases secretion of dietary triglyceride into lymph.Physiological reports · 2014Article
- Apolipoproteins C-I and C-III inhibit lipoprotein lipase activity by displacement of the enzyme from lipid droplets.The Journal of biological chemistry · 2013Article
- The regulation of ApoB metabolism by insulin.Trends in endocrinology and metabolism: TEM · 2013Review
- Changes in helical content or net charge of apolipoprotein C-I alter its affinity for lipid/water interfaces.Journal of lipid research · 2013Article
- Lipoprotein metabolism in nonalcoholic fatty liver disease.Journal of biomedical research · 2013Article
- Hepatic ABCA1 and VLDL triglyceride production.Biochimica et biophysica acta · 2012Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
We have shown that expression of apolipoprotein (apo) C-III promotes VLDL secretion from transfected McA-RH7777 cells under lipid-rich conditions. To determine structural elements within apoC-III that confer to this function, we contrasted wild-type apoC-III with a mutant Ala23Thr originally identified in hypotriglyceridemia subjects. Although synthesis of [(3)H]glycerol-labeled TAG was comparable between cells expressing wild-type apoC-III (C3wt cells) or Ala23Thr mutant (C3AT cells), secretion of [(3)H]TAG from C3AT cells was markedly decreased. The lowered [(3)H]TAG secretion was associated with an inability of C3AT cells to assemble VLDL(1). Moreover, [(3)H]TAG within the microsomal lumen in C3AT cells was 60% higher than that in C3wt cells, yet the activity of microsomal triglyceride-transfer protein in C3AT cells was not elevated. The accumulated [(3)H]TAG in C3AT microsomal lumen was mainly associated with lumenal IDL/LDL-like lipoproteins. Phenotypically, this [(3)H]TAG fractionation profiling resembled what was observed in cells treated with brefeldin A, which at low dose specifically blocked the second-step VLDL(1) maturation. Furthermore, lumenal [(35)S]Ala23Thr protein accumulated in IDL/LDL fractions and was absent in VLDL fractions in C3AT cells. These results suggest that the presence of Ala23Thr protein in lumenal IDL/LDL particles might prevent effective fusion between lipid droplets and VLDL precursors. Thus, the current study reveals an important structural element residing within the N-terminal region of apoC-III that governs the second step VLDL(1) maturation.
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Registered trials
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