APOB


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APOB

A gene on chromosome 2p24-p23 that encodes apolipoprotein B, the main apoliprotein of chylomicrons and low-density lipoproteins, which appears in plasma as two main isoforms: apoB48 (which is synthesised exclusively in the gut) and apoB100 (which is synthesised in the liver).

Molecular pathology
APOB mutations cause hypobetalipoproteinaemia, normotriglyceridemic hypobetalipoproteinaemia, and hypercholesterolaemia due to ligand-defective apoB.
References in periodicals archive ?
The genotypes and allele frequencies of ApoB and ACE genes did not differ between trained and control groups (P > 0.05).
pylori infection may contribute to dyslipidemia by affecting ApoA1, ApoB, TG, TC, HDL, LDL, and oxidized LDL levels, and that these effects may promote the development of atherosclerosis [34-36].
ApoA-I, apoB, and apoC-III were determined by previously validated electroimmunoassays [21-23].
The distribution of S4338N polymorphism was found to be significantly different in CHD and control groups (P = 0.0008; RR (95% CI) = 0.685 (0.543, 0.864); Odds Ratio (95% CI) = 0.486 (0.319, 0.739), suggesting that S4338N polymorphism in ApoB gene may have minor contribution in early development of coronary heart disease and therefore can be considered as a genetic marker for disease risk assessment.
No significant differences were observed for either group with apoB concentrations.
Mice, humans and other mammals produce a directly analogous protein called apolipoprotein B (apoB) and therapies have been developed to reduce apoB to prevent cardiovascular disease.
Beyond LDL-C, both non-HDL-C and apolipoprotein B (ApoB) are considered important lipid markers for not only LDL particles but also for TG-rich lipoprotein concentrations, CVD risk prediction, and monitoring the efficacy of LLDs especially in patients with DM and MetS.
Recent findings have helped to further clarify the regulatory steps in VLDL metabolism in the liver in type 2 diabetes n normal subjects, insulin inhibits the assembly and secretion of VLDL particles by increasing apolipoprotein B (apoB) degradation and decreasing the expression of the microsomal transfer protein (MTP) in hepatocytes.
BMI, waist circumference, sum of 4 skinfolds, TG, glucose, HOMA, C-reactive protein (CRP), APOA1, APOB, and leptin were skewed and therefore log-transformed before z-scores were constructed.
One of the most strongly selected genes is APOB, which in mammals encodes the main protein in LDL (low density lipoprotein), known widely as "bad" cholesterol.