ArticleThe Journal of biological chemistry2011
Missense mutation in APOC3 within the C-terminal lipid binding domain of human ApoC-III results in impaired assembly and secretion of triacylglycerol-rich very low density lipoproteins: evidence that ApoC-III plays a major role in the formation of lipid precursors within the microsomal lumen.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.
- Biotechnology Approaches for the Treatment of Dyslipidemia.Cardiovascular drugs and therapy · 2021Pooled it
- Associations of the APOC3 rs5128 polymorphism with plasma APOC3 and lipid levels: a meta-analysis.Lipids in health and disease · 2015Pooled it
- The Effects of Supplemented Conjugated Linoleic Acid on Lipid Metabolism in Cattle.Animals : an open access journal from MDPI · 2026Review
- ApoC-III proteoforms are associated with better lipid, inflammatory, and glucose profiles independent of total apoC-III.Cardiovascular diabetology · 2024Article
- Impaired Hepatic Very Low-Density Lipoprotein Secretion Promotes Tumorigenesis and Is Accelerated with Fabp1 Deletion.The American journal of pathology · 2024Article
- Review
- Article
- Exploring apolipoprotein C-III: pathophysiological and pharmacological relevance.Cardiovascular research · 2024Review
- Dysfunctional VLDL metabolism in MASLD.npj metabolic health and disease · 2024Review
- Broadening the Scope of Dyslipidemia Therapy by Targeting APOC3 (Apolipoprotein C3) and ANGPTL3 (Angiopoietin-Like Protein 3).Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Obstructive Sleep Apnoea and Lipid Metabolism: The Summary of Evidence and Future Perspectives in the Pathophysiology of OSA-Associated Dyslipidaemia.Biomedicines · 2022Review
- Plasma proteomics reveals crosstalk between lipid metabolism and immunity in dairy cows receiving essential fatty acids and conjugated linoleic acid.Scientific reports · 2022Article
- Apolipoprotein CIII Deficiency Protects Against Atherosclerosis in Knockout Rabbits.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- ApoE and apoC-III-defined HDL subtypes: a descriptive study of their lecithin cholesterol acyl transferase and cholesteryl ester transfer protein content and activity.Lipids in health and disease · 2020Article
- Nonalcoholic fatty liver disease experiences accumulation of hepatic liquid crystal associated with increasing lipophagy.Cell & bioscience · 2020Article
- Sequence analysis and variant identification at the APOC3 gene locus indicates association of rs5218 with BMI in a sample of Kuwaiti's.Lipids in health and disease · 2019Article
- Emerging evidences for the opposite role of apolipoprotein C3 and apolipoprotein A5 in lipid metabolism and coronary artery disease.Lipids in health and disease · 2019Review
- ApoC-III ASO promotes tissue LPL activity in the absence of apoE-mediated TRL clearance.Journal of lipid research · 2019Article
- Biomarkers and subtypes of deranged lipid metabolism in non-alcoholic fatty liver disease.World journal of gastroenterology · 2019Review
- Apolipoprotein C-III and its defined lipoprotein subspecies in relation to incident diabetes: the Multi-Ethnic Study of Atherosclerosis.Diabetologia · 2019Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic assembly of triacylglycerol (TAG)-rich very low density lipoproteins (VLDL) is achieved through recruitment of bulk TAG (presumably in the form of lipid droplets within the microsomal lumen) into VLDL precursor containing apolipoprotein (apo) B-100. We determined protein/lipid components of lumenal lipid droplets (LLD) in cells expressing recombinant human apoC-III (C3wt) or a mutant form (K58E, C3KE) initially identified in humans that displayed hypotriglyceridemia. Although expression of C3wt markedly stimulated secretion of TAG and apoB-100 as VLDL(1), the K58E mutation (located at the C-terminal lipid binding domain) abolished the effect in transfected McA-RH7777 cells and in apoc3-null mice. Metabolic labeling studies revealed that accumulation of TAG in LLD was decreased (by 50%) in cells expressing C3KE. A Fat Western lipid protein overlay assay showed drastically reduced lipid binding of the mutant protein. Substituting Lys(58) with Arg demonstrated that the positive charge at position 58 is crucial for apoC-III binding to lipid and for promoting TAG secretion. On the other hand, substituting both Lys(58) and Lys(60) with Glu resulted in almost entire elimination of lipid binding and loss of function in promoting TAG secretion. Thus, the lipid binding domain of apoC-III plays a key role in the formation of LLD for hepatic VLDL assembly and secretion.
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