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Hamster Monoclonal APOA5 Primary Antibody for ELISA, FACS - ABIN152906
Pennacchio, Olivier, Hubacek, Cohen, Cox, Fruchart, Krauss, Rubin: An apolipoprotein influencing triglycerides in humans and mice revealed by comparative sequencing. in Science (New York, N.Y.) 2001
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Human Polyclonal APOA5 Primary Antibody for ELISA, WB - ABIN543847
Luo, Kranzler, Zuo, Wang, Blumberg, Gelernter: CHRM2 gene predisposes to alcohol dependence, drug dependence and affective disorders: results from an extended case-control structured association study. in Human molecular genetics 2005
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Monoclonal APOA5 Primary Antibody for ELISA - ABIN534098
Prieur, Coste, Rodriguez: The human apolipoprotein AV gene is regulated by peroxisome proliferator-activated receptor-alpha and contains a novel farnesoid X-activated receptor response element. in The Journal of biological chemistry 2003
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Monoclonal APOA5 Primary Antibody for IHC (p), ELISA - ABIN534099
OBrien, Alborn, Sloan, Ulmer, Boodhoo, Knierman, Schultze, Konrad: The novel apolipoprotein A5 is present in human serum, is associated with VLDL, HDL, and chylomicrons, and circulates at very low concentrations compared with other apolipoproteins. in Clinical chemistry 2005
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Human Polyclonal APOA5 Primary Antibody for ELISA, WB - ABIN314229
Corella, Lai, Demissie, Cupples, Manning, Tucker, Ordovas: APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study. in Journal of molecular medicine (Berlin, Germany) 2007
Human Polyclonal APOA5 Primary Antibody for WB - ABIN2565346
van den Berg, Heemskerk, Geerling, van Klinken, Schaap, Bijland, Berbée, van Harmelen, Pronk, Schreurs, Havekes, Rensen, van Dijk: Apolipoprotein A5 deficiency aggravates high-fat diet-induced obesity due to impaired central regulation of food intake. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2013
the screening of APOA5 and APOC3 genotypes may be useful to estimate changes in triglyceride concentrations during bexarotene treatment in patients with CTCL and also to identify the best candidates for bexarotene therapy based on the expected adverse effect profile.
A missense variant at APOA5 gene is associated with coronary artery disease.
The association of risk allele C of genetic variant rs662799 of Apolipoprotein A5 gene with dyslipidaemia and obesity may lead to the development of metabolic syndrome in the Pakistan adult population.
Reductions in continuous Metabolic Syndrome score at both 3 months and 1 year were significantly associated with 2 variants: rs662799 (A/G) in apolipoprotein A5 (APOA5) and rs1501299 (G/T) in adiponectin (ADIPOQ).
APOA5 variation regulates triglyceride and HDL levels, thus displaying a causal role in the development of coronary artery disease.
APOA5 SNPs rs662799 and rs651821 exhibited significant differences in genotype and allele distributions between patients with coronary artery disease (CAD) and control subjects. SNP rs662799 was significantly correlated with increased risk of CAD when a dominant model was considered. The variants of the APOA5 gene are associated with CAD susceptibility and may modulate plasma triglyceride levels in a Chinese population.
Excess risk for low HDL-C and hyperlipidemia was associated with rs662799 genotype alleles of APOA5 SNPs in older Chinese adults.
ApoA5 can inhibit the adipogenic differentiation of AMSC,and this effect may be mediated by down-regulating the expression of CIDEC. Furthermore, our results indicate that CIDEC could be considered as a key factor in adipogenic differentiation.
TC+CC genotype of rs662799 is associated with high serum triglyceride and low LDL and BMI levels. In addition, the rs662799 C allele (TC+CC) is an independent protective factor for small vessel occlusion in the Han Chinese population in Taiwan.
Suggest that APOA5 SNPs rs10750097(G/G), rs1263173(A/A), rs17120035(T/T), and rs662799(G/G) may be associated with NAFLD.
Evidence has established the association between the presence of APOA5 gene SNPs and the risk for obesity. (Review)
Polymorphisms of the genes MTHFR (rs1801133) and APOA5 (rs662799), as well as anemia, are independent risk factors for stroke in Mexicans, together with traditional cardiovascular risk factors such as high triglycerides and high blood pressure.
Different linkage disequilibrium was found betweenAPOA5 rs207560 and rs3135506 variants in Roma compared to Hungarians
APOA5 polymorphisms rs662799 and rs3135507, with the CC and the AA genotypes, respectively, are associated with increased levels of both high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) in the Turkish Cypriot population.
rs670, rs2854116, and rs662799 single nucleotide polymorphisms of the APOA1-C3-A5 cluster are associated with ischemic stroke in the northern Chinese Han population.
The minor allele rs662799 in APOA5 was risk factor for coronary artery disease occurrence in the Chinese Han population.
Heterozygous carriers of the variants of APOA5 display more pronounced post-prandial lipemia after pure fat load than wild-type carriers.
Review/Meta-analysis: significant association of APOA5 rs662799 CC and APOA5 rs3135506 CG with increased risk of ischemic stroke.
The data clearly show that the Arg282Ser mutation in APOA5 gene determines a reduction of triglycerides, total and LDL-cholesterol and apolipoprotein A-V levels in overweight/obese children and adolescents, demonstrating that this mutation has the power to affect lipid levels already since childhood.
First study reporting the association of APOA5 gene variants with Metabolic Syndrome in Tunisia. This study emphasizes the role of APOA5 variants in the regulation of the triglycerides blood levels.
Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice.
lnc-RAP3 suppress 3T3-L1 preadipocyte differentiation by affecting the expression of the genes involved in adipogenic differentiation.
ApoA-V is a novel regulator of lipid metabolism in cardiomyocytes.
novel role for ApoA5 as a modulator of susceptibility to diet-induced liver and muscle insulin resistance through regulation of ectopic lipid accumulation in liver and skeletal muscle.
The data suggest that apoA-V suppresses the production of chylomicrons, playing a previously unknown role in lipid metabolism that may contribute to the postprandial hypertriglyceridemia associated with apoA-V deficiency.
Data indicate that apolipoprotein A5 (APOA5) plays a role in the central regulation of food intake.
Clearance of triglyceride-rich lipoproteins by hepatic SDC1 is atheroprotective and mediated by multivalent binding to ApoE and ApoAV.
Gene transfer of human apoA-V improves the severe hypertriglyceridemia phenotype of apoa5 null mice.
Intravenously injected apoA-V rHDL significantly lowers plasma TG in an apoA-V deficient mouse model and requires gpihbp1.
Data show that livers from apolipoprotein A-V (APOA-V) transgenic mice contain significantly higher amounts of triglycerides than livers from wild-type or apoA-V knockout mice, suggesting that apoA-V influences intrahepatic triglyceride levels.
Preferential association of apoA-V(1-146) with murine plasma HDL, but not with VLDL, suggests that particle size is a determinant of its lipoprotein binding specificity.
a role of ApoA-V in regulating levels of circulating triglycerides and cholesterol.
Review. APOA5 represents a newly discovered gene involved in triglyceride metabolism in both humans and mice whose mechanism of action remains to be deciphered.
apoAV lowers plasma TG by both reducing the hepatic VLDL-TG production rate and by enhancing the lipolytic conversion of TG-rich lipoproteins
ApoAIV is a direct target gene of Liver X receptors (LXRs) that may contribute to the antiatherogenic effect of LXR activation
apo A-IV and apo A-V are positive acute-phase proteins in mouse HDL.
apoAV reduces triglyceride levels by guiding VLDL and chylomicrons to proteoglycan-bound LPL for lipolysis
in staggerer mice, apoa5 gene is not affected by RORalpha
absence of apoAV slows lipolysis of triglyceride rick lipoprotein and the removal of their remnants by regulating their apoproteins content after secretion
These data demonstrate that (i) apoA-V expression decreases early during the APR due to changes in mRNA stability, and (ii) during the APR apoA-V is not inversely related to plasma TG levels in mice and humans.
gene polymorphisms in APOA5 and APOC3 are associated with meat quality traits in Kele pigs
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.
, apolipoprotein AV
, apolipoprotein A5
, regeneration-associated protein 3