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 ?
Biotherapeutics company CSL Behring reported on Friday the first patient enrolment under the first clinical trial AEGIS-II (ApoA-I Event reducinG in Ischemic Syndromes II) following an acute myocardial infarction (MI) and cardiovascular disease, which is the leading cause of death globally.
using a "pre-[beta]1-specific" monoclonal primary antibody (mab55201) for detecting apoA-I in pre-[beta]1-HDL (13).
Depletion of Rab8 in foam cell inhibits cholesterol efflux to apoA-I in part by the reduction of ABCA1 level at the PM [46].
As the major protein component of plasma HDL, apolipoprotein A-I (ApoA-I) synthesized in the liver and small intestine has been reported to be associated with clinical survival in multiple human cancers, including gastric cancer, nasopharyngeal carcinoma, and breast cancer [14-17].
Besides combined interventions to further increase the LDL-C lowering potential, it can be considered to target at the same time other CHD risk parameters including serum high density lipoprotein (HDL) cholesterol (HDL-C), apolipoprotein A-I (apoA-I), triacylglycerol or lipoprotein(a) concentrations, and/or blood pressure [5].
High-density lipoprotein (HDL) and apolipoprotein A-I (apoA-I), the main proteins of HDL, are antiatherogenic, cardioprotective, and exhibit anti-inflammatory properties.
In endothelial cells, apoA-I binding to ATPase-B1 causes ATP synthase to hydrolyze ATP into ADP and inorganic phosphate.
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.