ApoA1 Antibody [L13J2] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Human small intestine, Lane 2: Human plasma

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
25 kDa

Positive Control	HepG2 concentrated media
Negative Control	HepG2 cells

Datasheet & SDS

Biological Description

Specificity
ApoA1 Antibody [L13J2] detects endogenous levels of total ApoA1 protein.

Clone
L13J2

Synonym(s)
Apolipoprotein A-I; Apo-AI; ApoA-I; Apolipoprotein A1; APOA1

Background
Apolipoprotein A-I (ApoA-I) is the primary structural and functional protein of high-density lipoprotein (HDL), synthesized mainly in the liver and intestine to mediate reverse cholesterol transport by facilitating ABCA1-dependent cholesterol efflux from peripheral tissues to the liver for excretion, thereby offering protection against atherosclerosis and cardiovascular disease. The mature 243-amino-acid ApoA-I polypeptide comprises 10 tandem repeats of amphipathic α-helices, with proline residues providing flexibility for lipid binding; its N-terminal region stabilizes the lipid-free form, the central domain (140–170) activates lecithin-cholesterol acyltransferase (LCAT) for cholesterol esterification and HDL maturation, and the C-terminal domain (181–243) enables high-affinity phospholipid binding for nascent HDL formation. ApoA-I serves as a cofactor for LCAT, interacts with ABCA1 and SR-BI receptors to promote lipid efflux, and exhibits strong anti-inflammatory and antioxidant actions by neutralizing lipopolysaccharides and inhibiting vascular adhesion molecule expression. Low ApoA-I levels are an independent risk predictor for coronary artery disease, while APOA1 mutations cause familial HDL deficiency syndromes or hereditary amyloidosis, leading to accelerated atherosclerosis or organ dysfunction from protein deposits, with additional links to Alzheimer’s disease and diabetes through impaired lipid homeostasis and chronic inflammation.

Background

Apolipoprotein A-I (ApoA-I) is the primary structural and functional protein of high-density lipoprotein (HDL), synthesized mainly in the liver and intestine to mediate reverse cholesterol transport by facilitating ABCA1-dependent cholesterol efflux from peripheral tissues to the liver for excretion, thereby offering protection against atherosclerosis and cardiovascular disease. The mature 243-amino-acid ApoA-I polypeptide comprises 10 tandem repeats of amphipathic α-helices, with proline residues providing flexibility for lipid binding; its N-terminal region stabilizes the lipid-free form, the central domain (140–170) activates lecithin-cholesterol acyltransferase (LCAT) for cholesterol esterification and HDL maturation, and the C-terminal domain (181–243) enables high-affinity phospholipid binding for nascent HDL formation. ApoA-I serves as a cofactor for LCAT, interacts with ABCA1 and SR-BI receptors to promote lipid efflux, and exhibits strong anti-inflammatory and antioxidant actions by neutralizing lipopolysaccharides and inhibiting vascular adhesion molecule expression. Low ApoA-I levels are an independent risk predictor for coronary artery disease, while APOA1 mutations cause familial HDL deficiency syndromes or hereditary amyloidosis, leading to accelerated atherosclerosis or organ dysfunction from protein deposits, with additional links to Alzheimer’s disease and diabetes through impaired lipid homeostasis and chronic inflammation.

References
https://pubmed.ncbi.nlm.nih.gov/10828078/ https://pubmed.ncbi.nlm.nih.gov/27382195/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%