Apolipoprotein B (APOB) ELISA Kits

Human Apolipoprotein B (APOB) interaction partners

1. This study shows that the ApoB-516C/T promoter gene polymorphism has no impact on the risk of hepatitis C virus infection. However, the C/T genotype may be a protective factor for females.

2. association of TM6SF2 rs58542926 genotype with increased serum tyrosine levels and decreased apoB-100 particles in Finns

3. that apos involved in TG metabolism such as apoC2 (show APOC2 ELISA Kits), C3, E, and A4 (micromolar concentration), and apoB48 and apoA5 (show APOA5 ELISA Kits) (single-digit nanomolar concentration) can be quantified from a single digestion mixture.

4. These findings indicate that maternal apo (show C9orf3 ELISA Kits) B levels are significantly associated with apo (show C9orf3 ELISA Kits) B levels in their pre-school age children, adjusted for confounding variables. Furthermore, the mother-child correlations in apo (show C9orf3 ELISA Kits) B levels were independent of mother-child adiposity. Measurement of apo (show C9orf3 ELISA Kits) B levels in mothers may identify both high-risk children and mothers who may benefit from intervention.

5. Individuals with apoB higher than predicted by non-HDL (show HSD11B1 ELISA Kits)-C had significantly higher levels of PAI-1 (show SERPINE1 ELISA Kits), which may contribute to the increased risk of future atherothrombotic events

6. analysis of five likely pathogenic heterozygous rare variants that include four novel nonsense mutations in APOB (p.Gln845*, p.Gln2571*, p.Cys2933* and p.Ser3718*) and a rare variant in PCSK9 (show PCSK9 ELISA Kits) (Minor Allele Frequency <0.1%).

7. The impact of smoking on the levels of apolipoprotein B (APOB) was evaluated by analyzing data from NHANES for the years 2007-2012 for US adolescents aged 12-19 years and adults aged greater than or eqult to 20 years. The study found that smoking did not influence the observed levels of APOB for either adolescents or adults.

8. Identify LDLR (show LDLR ELISA Kits), APOB and PCSK9 (show PCSK9 ELISA Kits) novel mutations causing familial hypercholesterolemia in the central south region of China.

9. Rare variants of APOB or PCSK9 (show PCSK9 ELISA Kits) were identified in nine of the 22 study patients with extremely low LDL-C levels

10. Eicosapentaenoic acid has direct antioxidant benefits in various apoB-containing subfractions.

Mouse (Murine) Apolipoprotein B (APOB) interaction partners

1. enhanced VLDL TG secretion in the absence of hepatocyte ABCA1 (show ABCA1 ELISA Kits) is due to altered intracellular trafficking of apolipoprotein B (apoB), resulting in augmented TG addition to nascent VLDL.

2. We carried out our experiment in mice deficient in the low density lipoprotein (LDL) receptor (show LDLR ELISA Kits) and expressing only ApoB100 molecule (ApoB - LDLr (show LDLR ELISA Kits)) where the development of atherosclerosis is known to closely mimic human atherosclerosis

3. The effect of hypercholesterolemia induced immune response and inflammation on progression of atherosclerosis in ApoB(tm25gy) LDLr (show LDLR ELISA Kits)(tm1Her) mice, expressing only ApoB100 and deficient in the low density lipoprotein receptor (show LDLR ELISA Kits).

4. ApoB-containing lipoproteins contribute to augmentation of AngII-induced abdominal aortic aneurysms in male mice.

5. Immunization with human apolipoprotein B100 (ApoB) resulted in four-fold increased accumulation of effector T cells in ApoB-containing matrigel

6. PCSK9 (show PCSK9 ELISA Kits) markedly increases intestinal triglyceride-rich apoB production through mechanisms mediated in part by transcriptional effects on apoB.

7. Mice that produce apoB100 in the RPE and liver secrete lipoproteins into Bruch's membrane, but not to the extent that distinct features of AMD (show AMD1 ELISA Kits) develop

8. The aim of this study was to characterize the ocular morphology of low-density lipoprotein receptor-deficient apolipoprotein B-100-only mice, with IGF-II overexpression.

9. Our data establish the role of APOB gene in severe gut (show GUSB ELISA Kits) dysmotility.

10. Cardiac lipotoxicity may originate from direct inhibition of myocardial ApoB lipoprotein and subsequent decreased lipid export, caused by supraphysiological levels of catecholamines.

Cow (Bovine) Apolipoprotein B (APOB) interaction partners

1. The clinicopathological phenotype of affected Holstein cattle homozygous for the causative apolipoprotein B gene (APOB) mutation associated with cholesterol deficiency is described.

2. Beyond malabsorption of dietary lipids, deleterious effects of apolipoprotein B deficiency on hepatic lipid metabolism, steroid biosynthesis, and cell membrane function can be expected, which may result in unspecific symptoms of reduced fertility, growth, and health.

3. Cholesterol deficiency results from a 1.3kbp insertion of an endogenous retrovirus (ERV2-1-LTR_BT) into exon 5 of the APOB gene at BTA11:77,959kb. The insertion is flanked by 6bp target site duplications as described for insertions mediated by retroviral integrases.

4. A transposable element insertion in APOB causes cholesterol deficiency in Holstein cattle

5. Nonesterified fatty acids significantly inhibit the expression of ApoB100, ApoE (show APOE ELISA Kits), MTP (show MTTP ELISA Kits), and LDLR (show LDLR ELISA Kits), thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.

6. after calving the apolipoprotein B(100) mRNA synthesis was lower, whereas microsomal triglyceride transfer protein (MTP (show MTTP ELISA Kits)) and apolipoprotein E (show APOE ELISA Kits) messenger RNA abundance were higher in the liver.

Pig (Porcine) Apolipoprotein B (APOB) interaction partners

1. found association between genotypes for LDLR (show LDLR ELISA Kits) and APOB polymorphisms and serum lipid levels, but none of them seem to be the causal mutation but probably represent closely linked polymorphisms