APOA1

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 ?
Table-II: show Pearson correlation between PON1 enzyme level and LDL, HDL, apoA1 and apo B in T1DM and T2DM.
All measured biomarkers, except LDL-C, showed improvement: "Intention-to-treat analysis (% change) revealed the following at 1-year: total LDL-particles (LDL-P) (-4.9%, P=0.02), small LDL-P (-20.8%, P=1.2 x [10.sup.-12]), LDL-P size (+1.1%), ApoB (-1.6%), ApoA1 (+9.8%), ApoB/ApoA1 ratio (-9.5%), triglyceride/HDL-C ratio (-29.1%), large VLDL-P (-38.9%), and LDL-C (+9.9%)." The authors note that LDL-C, regarded as a CVD risk factor, has also been inversely correlated with mortality in two large prospective studies.
The large global INTERHEART study in 52 countries indicated that smoking, exercise, fruit and vegetable intake, alcohol, hypertension, diabetes, abdominal obesity, psychosocial factors, and high apolipoprotein B100 (ApoB)/apolipoprotein A1 (ApoA1) ratio were associated with AMI.[6],[7] In addition to ApoB/ApoA1, Karthikeyan et al .[3] investigated the role of other lipid indexes of AMI risk in the Asian population.
FRIDAY, May 11, 2018 (HealthDay News) -- Self-assembling peptide amphiphile (PA) nanofibers, incorporating an 18 amino acid sequence that retains the cholesterol efflux actions of apolipoprotein-A1 (apoA1) and a liver X receptor (LXR) agonist can target and treat atherosclerosis, according to an experimental study presented at the American Heart Association's Vascular Discovery: From Genes to Medicine Scientific Sessions 2018, held from May 10 to 12 in San Francisco.
1993) constructs were used to test RXR activation using the reporter tk-(ApoA1)x4-luc (Blumberg et al.
In the analysis, we found that the total intake of fat, as well as the individual intake of each type of fat was associated with a higher concentration of total cholesterol and LDL-cholesterol, but also with higher levels of HDL-cholesterol and apolipoprotein A1 (ApoA1) and lower levels of Triglycerides, Total Cholesterol / HDL-cholesterol ratio, Triglycerides / HDL cholesterol ratio and the apolipoprotein B (ApoB) / ApoA1 ratio (all with a p trend <0.0001).
As expected, the MetS patients had significantly increased glucose, triglycerides, waist circumference, systolic and diastolic blood pressures, BMI, insulin, HOMA-IR, total cholesterol, LDL cholesterol, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), and serum leptin levels in comparison to the non-MetS subjects, whereas high-density lipoprotein (HDL) cholesterol, ApoA1, and adiponectin values were significantly lower compared with the non-MetS subjects.
ApoA1 and A2 on HDL stimulate the enzyme LCAT, which then esterifies the cell surface cholesterol molecules to form cholesteryl ester, which migrate to the core of the HDL particle to form mature migrating HDL[2].
Genes in Genes in the Percentage Fold our analysis FunRich of genes enrichment database Exosomal 37 2001 72.54 5.26 proteins A1BG, ACTA1, ACTA2, ACTB, ACTBL2, ACTC1, ACTG1, ACTG2, ALB, AMBP, APOA1, APOD, AZGP1, B2M, CDH1, CLU, CP, CRNN, DCTN2, EGF, HP, HPR, HSPB1, ITIH4, KNG1, LAMA3, LMAN2, POTEE, POTEF, POTEI, S100A8, SERPINA1, SERPING1, TF, TTR, UMOD, and VASN.
During lipid metabolism, (1) TMAO significantly increases the expression of ABCA1 and ABCG1 in the liver which helps cholesterol efflux to apoA1 as the cholesterol acceptor; (2) TMAO in the gut also markedly reduces the mRNA expression of NPC1L1, which transports cholesterol into the enterocyte from the gut lumen; (3) TMAO reduces the bile acid pool in the liver, which is associated with the classic RCT by reducing synthetic enzymes CYP7A1 and CYP27A1; and (4) TMAO also reduces the expression of ABCG5/8 in the TICE pathway.
They also maintained that irisin, first discovered in 2012, was actually Apolipoprotein A1 (ApoA1), with the same molecular size, measured in plasma.
Similarly, other apolipoproteins, such as ApoJ, and ApoA1, might also associate with [alpha]S to modify evolvability [37, 38].