APOA1

(redirected from apoA-I)

APOA1

A gene on chromosome 11q23-q24 that encodes apolipoprotein A1, the main protein component of high-density lipoprotein (HDL) in plasma, which promotes cholesterol efflux from tissues to the liver for excretion and is a cofactor for lecithin cholesterolacyltransferase (LCAT), which is responsible for forming most plasma cholesteryl esters.
 
Molecular pathology
APOA1 mutations cause HDL deficiency (e.g., Tangier disease and systemic non-neuropathic amyloidosis).
References in periodicals archive ?
Longevity Biotech Inc, a biopharmaceutical company that develops therapeutic drug candidates, has received a USD225,000 Phase I SBIR Contract from the National Heart, Lung, and Blood Institute, a division of the National Institutes of Health, for the development of the 5A apoA-I mimetic peptide program intended for the treatment of severe asthma, it was reported yesterday.
En este sentido, citoquinas pro-inflamatorias como TNF-[alpha] e IL-6 disminuyen la expresion de ApoA-I e inducen la expresion de la proteina amiloide A serica (SAA), la cual cambia la composicion de las HDL (20), afectando su capacidad antiinflamatoria y antioxidante (21).
RCT begins in the liver and intestines with the synthesis of apolipoproteins (apo; primarily the apoA-I subtype).
ApoA-I mimetic peptide 4F, which contains only 18 amino acids and contains a Class A amphipathic helix with a polar and a nonpolar face that allows it to bind lipids similar to apoA-I.
In this study, the scientists show that apoA-I binding protein (AIBP) is secreted by surrounding tissues and facilitates cholesterol removal from endothelial cells.
Here, I propose to study the potential role of apoA-I in regulating the function of conventional and regulatory T cells.
The 299-patient, 12-week, randomized, double-blind ApoA-I Synthesis Stimulation Evaluation in Patients Requiring Treatment for Coronary Artery Disease (ASSERT) trial showed that the investigational oral small-molecule RVX-208 achieved dose-dependent increases in apoA-I, HDL, and highly efficient and cardioprotective large-size HDL particles.
The researchers found that very high HDL levels and very large HDL particles increased the risk of coronary artery disease when levels of apoA-I and apolipoprotein B (apoB, a component of LDL "bad" cholesterol) remained steady.
The first four chapters deal with the structures and properties of the HDL proteins apoA-I, -A-II, -E, and -M.
ApoA-I level and paraoxonase activity did not change; however, platelet-activating factor acetylhydrolase activity increased (P < 0.