APOA2

(redirected from ApoA-II)

APOA2

A gene on chromosome 1q21-q23 that encodes apolipoprotein A2, a protein component of high-density lipoprotein (HDL), which is present in plasma as a monomer, homodimer or heterodimer with apolipoprotein D.

Molecular pathology
APOA2 mutations cause apolipoprotein A2 deficiency or hypercholesterolaemia.
Mentioned in ?
References in periodicals archive ?
Indeed, in such a cohort, apoA-II influenced apoE-linked cardiovascular disease in Dutch women with high levels of HDL-cholesterol and C-reactive protein (13).
ApoA-I], and ApoA-II were not available in the WHS study (13) to investigate the influence of these variables on HDL size.
ApoA-II mRNA has been shown to be induced in human hepatocytes via PPAR activation (10).
Protein heterogeneity of lipoprotein particles containing apoA-I without apoA-II and apoA-I with apoA-II isolated from human plasma.
ApoA-II maintains HDL levels in part by inhibition of hepatic lipase: studies in apoA-II and hepatic lipase double knockout mice.
Analysis of HDL apolipoproteins and lipids was done on serum stored at -80[degrees]C after apolipoprotein-B (apoB)-containing lipoproteins were removed by precipitation using dextran-sulfate on beads (Polymedco), followed by analysis of the supernatant on Cobas-Fara (Roche) for apoA-I, apoA-II, apoE, triglycerides, total cholesterol, free cholesterol, and phospholipids (Wako Chemicals).
This finding is important, because prior data have suggested that apoA-II has poor antiatherogenic properties and may even be proatherogenic.
The second most abundant protein in HDL is apoA-II, and controversy exists regarding the role of apoA-II in cardiovascular risk.
ProteinChip technology: a new and facile method for identification and measurement of high-density lipoproteins apoA-I and apoA-II and their glycosylated products in patients with diabetes and cardiovascular disease.
ApoA-II was determined on the same system with N-antiserum against human ApoA-II from Dade-Behring (polyclonal; prod.
apolipoprotein (ApoA-I, ApoA-II, ApoB, ApoC-III, and ApoE, attaining 12.
In addition, the plasma of other mouse models of hyperlipidemia and atherosclerosis, such as human apoA-II transgenic mice or mice deficient in LDL receptor, presented similar interferences (data not shown).