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Apolipoprotein C-III

Apolipoprotein C-III, apoC-III, APOC3
Apolipoprotein C-III is a very low density lipoprotein (VLDL) protein. APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to delay catabolism of triglyceride-rich particles. The APOA1, APOC3 and APOA4 genes are closely linked in both rat and human genomes. The A-I and A-IV genes are transcribed from the same strand, while the A-1 and C-III genes are convergently transcribed. An increase in apoC-III levels induces the development of hypertriglyceridemia. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HDL, Apo, HAD, apolipoprotein B, apolipoprotein E
Papers using Apolipoprotein C-III antibodies
Fibrates down-regulate hepatic scavenger receptor class B type I protein expression in mice
Supplier
Oliveira Helena CF et al., In Lipids in Health and Disease, 2002
... CETP and apoCIII transgenic mice were crossbred to ...
Hypertriglyceridemia but not diabetes status is associated with VLDL containing apolipoprotein CIII in patients with coronary heart disease
Supplier
Borén Jan et al., In Diabetes, 2002
... Apolipoprotein C-III isofocusing in the diagnosis of genetic defects in O-glycan biosynthesis ...
Papers on Apolipoprotein C-III
Multiplexed peptide analysis for kinetic measurements of major human apolipoproteins by LC/MS/MS.
New
Nobécourt et al., France. In J Lipid Res, Feb 2016
UNASSIGNED: A multiplexed assay was developed by mass spectrometry to analyze in a single run six major human apolipoproteins (Apos) involved in lipoprotein metabolism: ApoAI, ApoAII, ApoB100, ApoCII, ApoCIII, and ApoE.
Impact of phosphatidylcholine liposomes on the compositional changes of VLDL during lipoprotein lipase (LPL)-mediated lipolysis.
New
Jankowski et al., Gdańsk, Poland. In Chem Phys Lipids, Feb 2016
UNASSIGNED: Lipoprotein lipase (LPL)-mediated triacylglycerol (TAG) hydrolysis in very low density lipoprotein (VLDL) is accompanied by the release of surface material containing phospholipids (PL), free cholesterol (FC) and apolipoproteins, E (apoE) and Cs (apoCII, apoCIII).
Gene-based therapies in lipidology: current status and future challenges.
New
Brisson et al., Montréal, Canada. In Curr Opin Lipidol, Dec 2015
Most advanced antisense oligonucleotide drugs target apolipoprotein C-III, apolipoprotein (a), angiopoietin-like 3, and diacylglycerol o-acyltransferase-2.
Genetics of coronary heart disease: towards causal mechanisms, novel drug targets and more personalized prevention.
Review
New
Orho-Melander, Malmö, Sweden. In J Intern Med, Nov 2015
Furthermore, identification of rare loss-of-function variants in genes such as PCSK9, NPC1L1, APOC3 and APOA5, which cause a markedly decreased risk of CHD and no adverse side effects, illustrates the power of translating genetic findings into novel mechanistic information and provides some optimism for the future of developing novel drugs, given the many genes associated with CHD in GWASs.
JCL roundtable: Apolipoproteins as causative elements in vascular disease.
Review
New
Sniderman et al., Atlanta, United States. In J Clin Lipidol, Nov 2015
Furthermore, the content of apoC3 in apoB-containing lipoproteins can predict risk without a close association with triglycerides or cholesterol.
Apolipoprotein C-III: From Pathophysiology to Pharmacology.
Review
New
Catapano et al., Milano, Italy. In Trends Pharmacol Sci, Oct 2015
Apolipoprotein C-III (apoC-III) has a critical role in the metabolism of triglyceride (TG)-rich lipoproteins (TRLs).
Antisense Inhibition of Apolipoprotein C-III in Patients with Hypertriglyceridemia.
New
Impact
Kastelein et al., Montréal, Canada. In N Engl J Med, Aug 2015
BACKGROUND: Apolipoprotein C-III (APOC3) is a key regulator of plasma triglyceride levels.
The risk of cardiovascular events with increased apolipoprotein CIII: A systematic review and meta-analysis.
Review
New
Sacks et al., Milwaukee, United States. In J Clin Lipidol, Jul 2015
BACKGROUND: Apolipoprotein CIII (apoC-III) is an atherogenic protein found on HDL, VLDL and LDL.
Analysis of loss-of-function variants and 20 risk factor phenotypes in 8,554 individuals identifies loci influencing chronic disease.
New
Impact
Boerwinkle et al., Houston, United States. In Nat Genet, Jun 2015
To test this hypothesis, we sequenced the exomes of 8,554 individuals and analyzed the effects of predicted LOF variants on 20 chronic disease risk factor phenotypes. Analysis of this sample as discovery and replication strata of equal size verified two relationships in well-studied genes (PCSK9 and APOC3) and identified eight new loci.
Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction.
New
Impact
Kathiresan et al., Boston, United States. In Nature, Mar 2015
Recent evidence has connected MI risk with coding-sequence mutations at two genes functionally related to APOA5, namely lipoprotein lipase and apolipoprotein C-III (refs 18, 19).
Targeting APOC3 in the familial chylomicronemia syndrome.
Impact
Witztum et al., Montréal, Canada. In N Engl J Med, 2015
Apolipoprotein C-III (APOC3) is known to inhibit LPL, although there is also evidence that APOC3 increases the level of plasma triglycerides through an LPL-independent mechanism.
Apolipoprotein CIII overexpression exacerbates diet-induced obesity due to adipose tissue higher exogenous lipid uptake and retention and lower lipolysis rates.
de Oliveira et al., Campinas, Brazil. In Nutr Metab (lond), 2014
We have previously observed an increased adiposity in response to a high fat diet (HFD) in mice overexpressing apoCIII.
Amyloid-Forming Properties of Human Apolipoproteins: Sequence Analyses and Structural Insights.
Review
Gursky et al., Boston, United States. In Adv Exp Med Biol, 2014
Surprisingly, the rank order of the amino acid sequence propensity to form amyloid (apoB>apoA-II>apoC-II≥apoA-I, apoC-III, SAA, apoC-I>apoA-IV, apoA-V, apoE) does not correlate with the proteins' involvement in amyloidosis.
APOA5 -1131T>C and APOC3 -455T>C polymorphisms are associated with an increased risk of coronary heart disease.
Chen et al., Beijing, China. In Genet Mol Res, 2014
The aim of this study was to investigate correlations between apolipoprotein A-V (APOA5) -1131T>C and apolipoprotein C-III (APOC3) -455T>C polymorphisms and coronary heart disease (CHD).
APOC3, coronary disease, and complexities of Mendelian randomization.
Impact
Hobbs et al., Dallas, United States. In Cell Metab, 2014
Two new studies report that triglyceride (TG)-lowering mutations in APOC3 reduce coronary heart disease (CHD) (Crosby et al., 2014; Jørgensen et al., 2014).
Genetic variation in PNPLA3 but not APOC3 influences liver fat in non-alcoholic fatty liver disease.
GeneRIF
Yki-Järvinen et al., Helsinki, Finland. In J Gastroenterol Hepatol, 2012
Genetic variants in PNPLA3 but not APOC3 contribute to the variance in liver fat content due to non-alcoholic fatty liver disease.
Females with angina pectoris have altered lipoprotein metabolism with elevated cholesteryl ester transfer protein activity and impaired high-density lipoproteins-associated antioxidant enzymes.
GeneRIF
Cho et al., Kyŏngsan, South Korea. In Int J Mol Med, 2012
The lipoprotein fractions in the angina pectoris group had impaired antioxidant activity and increased triglycerides and apoC-III with structural and functional changes.
Antisense inhibition of apoB synthesis with mipomersen reduces plasma apoC-III and apoC-III-containing lipoproteins.
GeneRIF
Sacks et al., Boston, United States. In J Lipid Res, 2012
Antisense inhibition of apoB synthesis reduced plasma concentrations of apoC-III and apoC-III-containing lipoproteins.
Identification of proteomic biomarkers in maternal plasma in the early second trimester that predict the subsequent development of gestational diabetes.
GeneRIF
Syn et al., Seoul, South Korea. In Reprod Sci, 2012
Data suggest that APOC3 is up-regulated as early as the second trimester in women developing gestational diabetes.
Mdm2 is a novel activator of ApoCIII promoter which is antagonized by p53 and SHP inhibition.
GeneRIF
Wang et al., Salt Lake City, United States. In Biochem Biophys Res Commun, 2012
Mdm2 inhibited p53-mediated enrichment of HNF4alpha to the ApoCIII promoter while simultaneously reducing p53 binding and increasing recruitment of SHP to the ApoCIII promoter.
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