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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Apolipoprotein A-V

APOA5, apolipoprotein A5, apoAV, apolipoprotein A-V
The protein encoded by this gene is an apolipoprotein that plays an important role in regulating the plasma triglyceride levels, a major risk factor for coronary artery disease. It is a component of high density lipoprotein and is highly similar to a rat protein that is upregulated in response to liver injury. Mutations in this gene have been associated with hypertriglyceridemia and hyperlipoproteinemia type 5. This gene is located proximal to the apolipoprotein gene cluster on chromosome 11q23. Alternatively spliced transcript variants encoding the same protein have been identified. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: HAD, HDL, Lipoprotein Lipase, AGE, Apolipoprotein C-III
Papers on APOA5
Association of Apolipoprotein A5 Gene Polymorphisms with Metabolic Syndrome in the Korean Population.
Hong et al., Cheju, South Korea. In Genet Test Mol Biomarkers, Feb 2016
AIMS: Functional defects of the ApoA5 protein have been identified is risk factors for hypertriglyceridemia, vascular diseases and susceptibility to metabolic syndrome (MetS).
Common genetic variants and subclinical atherosclerosis: The Multi-Ethnic Study of Atherosclerosis (MESA).
Bluemke et al., Washington, D.C., United States. In Atherosclerosis, Jan 2016
In HIS, CAC was associated with SNPs in 9p21 (rs1333049, P = 8 × 10(-5); rs4977574, P = 5 × 10(-5)), APOA5 (rs964184, P = 2 × 10(-4)), and ADAMTS7 (rs7173743, P = 4 × 10(-4)).
A novel APOC2 gene mutation identified in a Chinese patient with severe hypertriglyceridemia and recurrent pancreatitis.
Gao et al., Shanghai, China. In Lipids Health Dis, Dec 2015
The coding regions of 5 candidate genes (namely LPL, APOC2, APOA5, LMF1, and GPIHBP1) were sequenced using genomic DNA from peripheral leucocytes.
Meta-analysis of lipid-traits in Hispanics identifies novel loci, population-specific effects, and tissue-specific enrichment of eQTLs.
Valladares-Salgado et al., Houston, United States. In Sci Rep, Dec 2015
Genome-wide significant signals were observed in or near CELSR2, ZNF259/APOA5, KANK2/DOCK6 and NCAN/MAU2 for total cholesterol, LPL, ABCA1, ZNF259/APOA5, LIPC and CETP for HDL cholesterol, CELSR2, APOB and NCAN/MAU2 for LDL cholesterol, and GCKR, TRIB1, ZNF259/APOA5 and NCAN/MAU2 for triglycerides.
Update on the molecular biology of dyslipidemias.
Ramasamy, Worcester, United Kingdom. In Clin Chim Acta, Dec 2015
Monogenic hypertriglyceridemia is the result of mutations in genes that regulate the metabolism of triglyceride rich lipoproteins (eg LPL, APOC2, APOA5, LMF1, GPIHBP1).
Genetics of coronary heart disease: towards causal mechanisms, novel drug targets and more personalized prevention.
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.
Apolipoprotein A-V gene therapy for disease prevention / treatment: a critical analysis.
Ryan et al., Oakland, United States. In J Biomed Res, Nov 2015
It is hypothesized that individuals that manifest elevated plasma TG owing to deleterious APOA5 SNPs or rare mutations would respond to WT apoA-V supplementation with improved plasma TG clearance.
Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction.
Kathiresan et al., Boston, United States. In Nature, Mar 2015
At apolipoprotein A-V (APOA5), carriers of rare non-synonymous mutations were at 2.2-fold increased risk for MI.
Review APOA5 -1131T/C polymorphism and coronary artery disease susceptibility in Chinese population: an updated meta-analysis.
Zhang et al., Zhengzhou, China. In Genet Mol Res, 2014
Although many studies have investigated the association of the APOA5 -1131T/C polymorphism with coronary artery disease (CAD), definite conclusions have not been drawn.
Genetic predisposition of human plasma triglyceride concentrations.
Vrablik et al., Praha, Czech Republic. In Physiol Res, 2014
Rare mutations (mainly in the lipoprotein lipase and apolipoprotein C2) along with common polymorphisms (within apolipoprotein A5, glucokinase regulatory protein, apolipoprotein B, apolipo-protein E, cAMP responsive element binding protein 3-like 3, glycosylphosphatidylinositol-anchored HDL-binding protein 1) play an important role in determining plasma TG levels.
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).
Mutations in LPL, APOC2, APOA5, GPIHBP1 and LMF1 in patients with severe hypertriglyceridaemia.
Dallinga-Thie et al., Amsterdam, Netherlands. In J Intern Med, 2012
Mutations in GPIHBP1 are rare but the associated clinical phenotype of hypertriglyceridaemia is severe
-1131T>C and SW19 polymorphisms in APOA5 gene and lipid levels in type 2 diabetic patients.
Sousa et al., Belo Horizonte, Brazil. In Mol Biol Rep, 2012
APOA5 -1131T>C polymorphism is associated with decreased LDLc levels in subjects not treated with lipid lowering drugs; addition, the presence of the 19W allele from SW19 polymorphism is associated with higher triglyceride levels in type 2 diabetic patients
Synergistic effects of genetic variants of APOA5 and BTN2A1 on dyslipidemia or metabolic syndrome.
Yamada et al., Nagoya, Japan. In Int J Mol Med, 2012
Genetic variants of APOA5 and BTN2A1 may synergistically affect the prevalence of dyslipidemia in East Asian populations and of metabolic syndrome in Japanese individuals.
Vitamin D dependent effects of APOA5 polymorphisms on HDL cholesterol.
Hunt et al., Salt Lake City, United States. In Atherosclerosis, 2012
The rs3135506 minor allele was more strongly associated with low HDL-C in individuals with low winter dietary 25OHD in initial and replicate samples
Apolipoprotein A5 internalized by human adipocytes modulates cellular triglyceride content.
Liu et al., Changsha, China. In Biol Chem, 2012
Treatment of adipocytes with APOA5 significantly decreased cellular triglyceride storage.
Excess of rare variants in genes identified by genome-wide association study of hypertriglyceridemia.
Hegele et al., London, Canada. In Nat Genet, 2010
Through GWAS, we identified common variants in APOA5, GCKR, LPL and APOB associated with HTG.
Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies.
Danesh et al., Cambridge, United Kingdom. In Lancet, 2010
METHODS: We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease.
Newly identified loci that influence lipid concentrations and risk of coronary artery disease.
Abecasis et al., Ann Arbor, United States. In Nat Genet, 2008
Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol).
An apolipoprotein influencing triglycerides in humans and mice revealed by comparative sequencing.
Rubin et al., Berkeley, United States. In Science, 2001
an important determinant of plasma triglyceride levels
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