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Monoclonal APOA5 Primary Antibody für ELISA - ABIN534098
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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Hamster Monoclonal APOA5 Primary Antibody für ELISA, FACS - ABIN152906
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 für 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 für 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 für 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
APOA5 variants cause Hypertriglyceridemia. In high Cardiovascular risk patients APOA5 variants elevate triglyceride levels and shift the entire lipoprotein subclass distribution toward Atherogenic Dyslipidemia.
Triglyceride-raising variant alleles of the APOA5 encoding apo A (zeige APOA Antikörper)-V, associated with clinical Cardiovascular endpoints.
Hypertriglyceridemic patients carrying the APOA5 -1131T>C polymorphism exhibited increased atherogenic LDL levels and arterial stiffness, probably due to an effect of the -1131T>C polymorphism on apoA5 concentrations
The minor alleles of rs662799 (APOA5) and rs5072 (APOA1 (zeige APOA1 Antikörper)) modulate TG levels in Mexican children
Rare variants in LPL (zeige LCP1 Antikörper) and a common variant in APOA5 were more commonly found in Thai subjects with severe hypertriglyceridemia
Collectively, these data demonstrate that APOA5 SNP rs651821 might be an important host genetic factor in determining the abundances of the health-promoting Bifidobacterium bacteria and the taxa to which this genus belongs.
Data suggest that estrogen up-regulates serum concentrations of APOA5 and subsequently decreases serum triglyceride levels; APOA5 levels are higher in woman than in men, and the negative relationship between APOA5 and serum triglyceride levels is more significant in woman.
Methylation in exon 3 of APOA5 and epigenetic variability are associated with high circulating triacylglycerol levels.
the lead variant was the rs1558861 [1.99 (1.73-2.30); p = 7.37 x 10(-22) ], residing on chromosome (chr) 11 at the apolipoprotein A-I (zeige APOA1 Antikörper)/A-5 (APOA1 (zeige APOA1 Antikörper)/APOA5) locus
The single nucleotide polymorphisms in lipoprotein lipase (zeige LPL Antikörper), ApoA5, and CETP (zeige CETP Antikörper) were associated with serum triglycerides and HDL (zeige HSD11B1 Antikörper)-cholesterol levels, but not with coronary artery disease in Pakistani population under study.
novel role for ApoA5 as a modulator of susceptibility to diet-induced liver and muscle insulin (zeige INS Antikörper) 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 (zeige SDC1 Antikörper) is atheroprotective and mediated by multivalent binding to ApoE (zeige APOE Antikörper) 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 (zeige GPIHBP1 Antikörper).
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 (zeige HSD11B1 Antikörper), 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.
gene polymorphisms in APOA5 and APOC3 (zeige APOC3 Antikörper) 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