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 ?
KineMed's "Reverse Cholesterol Transport" FX-5A apoA-I high-density lipoprotein mimetic peptide is awarded a Rapid Access to Intervention Development (RAID) grant by the National Institute of Health
We have shown how HDL size can be combined with ApoA-I concentrations to estimate the concentration of HDL particles (HDL-P), and we briefly discuss the relevance of HDL size and HDL-P as biomarkers of CVD and diabetes.
Resverlogix's key focus, the NexVas Plaque Regression programme, seeks to develop new small molecules that boost ApoA-I production to address atherosclerosis, Acute Coronary Syndrome, Alzheimer's disease, peripheral artery disease and autoimmune diseases.
Also ceramide enhanced the binding of fluorescently labeled apoA-I to Chinese hamster ovary cells.
CER-001 is an innovative complex of recombinant human ApoA-I, the major structural protein of HDL, and phospholipids.
In parallel we estimated the abundance of apoA-I from the shotgun analysis using spectral counting and extracted ion chromatogram (XIC) peak areas for 2 peptides (20).
VIRxSYS will soon be initiating a non-human primate study to test the ability of our lead clinical candidate to raise serum apoA-I levels, leading to an increase in HDL.
VLDL apoB100 was isolated from the triglyceride-rich lipoprotein (TRL) fraction and apoA-I was isolated from the HDL fraction (density 1.
Donald McCaffrey, president and chief executive officer of Resverlogix, said that the company is now well positioned to advance RVX-208 to the next clinical trial having witnessed the substantial and consistent elevation of HDL by ApoA-I production, which strongly indicates that RVX-208 should remove unwanted plaque from the arterial wall, which is the main goal.
Crucial to these findings is the rapid onset of action in this 7 day trial, with the serum ApoA-I increases surpassing the previous 8% five week (35 day) average benchmark totals displayed by Pfizer's previous ApoA-I Milano recombinant protein studies.
ApoA-I and apoB were measured on a BNII nephelometer (Dade Behring/Siemens) according to the manufacturer's instructions.
Other objectives are to examine the safety and tolerability of RVX-208 and to compare the dose and time response relationship for ApoA-I as well as to examine key reverse cholesterol markers involved with HDL functionality.