Apolipoprotein A-i
Apolipoprotein A-i - Related Videos
07:36
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
0 Views •
Cited by 8 •
2018
We describe a protocol to induce atherosclerosis in the aortic root of ApoE-/- mice fed with an atherogenic diet, through a continuous release of aldosterone. Methods to characterize plaque composition are also described.
10:59
Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases
0 Views •
Cited by 32 •
2013
Recent development in gene targeting tools makes production of knockout (KO) rabbits possible. In the present work, we generated five Apolipoprotein (Apo) C-III KO rabbits using Zinc Finger Nucleases (ZFN). This work demonstrated that ZFN is a highly efficient method to produce KO rabbits.
07:37
Click-Chemistry Based Fluorometric Assay for Apolipoprotein N-acyltransferase from Enzyme Characterization to High-Throughput Screening
0 Views •
Cited by 2 •
2020
Presented here is a sensitive fluorescence assay to monitor apolipoprotein N-acyltransferase activity using diacylglyceryl peptide and alkyne-phospholipids as substrates with click-chemistry.
07:08
A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
0 Views •
Cited by 3 •
2016
We describe a high-throughput, multiplex, and targeted proteomic cerebrospinal fluid (CSF) assay developed with potential for clinical translation. The test can quantitate potential markers and risk factors for neurodegeneration, such as the apolipoprotein E variants (E2, E3 and E4), and measure their allelic expression.
02:23
RNA Editing
0 Views •
2020
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
FAQs
ABCA1 enables peripheral cells to transfer cholesterol and phospholipids to ApoA-I. This interaction supplies the lipid cargo needed for nascent HDL formation and allows excess cellular cholesterol to enter the transport pathway. Studying this step helps explain how cellular lipid balance is connected to HDL development and subsequent cholesterol handling.
ApoA-I activates lecithin–cholesterol acyltransferase, or LCAT, after cholesterol enters HDL. LCAT converts free cholesterol into cholesteryl esters, changing how the cholesterol is organized within the lipoprotein and supporting HDL maturation. This enzymatic interaction is therefore important for understanding how HDL continues processing cholesterol after its initial acquisition.
Esterification provides a further processing step for cholesterol carried by HDL. By converting free cholesterol into cholesteryl esters, the ApoA-I-dependent pathway supports the maturation of HDL and continued movement of cholesterol toward the liver. This connection links molecular enzyme activity with the broader biological process of reverse cholesterol transport.
Reverse cholesterol transport connects peripheral cellular cholesterol with hepatic processing and excretion. ApoA-I contributes to this pathway by supporting HDL formation, cholesterol acceptance, and LCAT activation. In biology research, this makes ApoA-I a useful focal point for examining how lipoprotein interactions influence whole-body cholesterol movement rather than isolated cellular lipid storage.
ApoA-I is studied as a biomarker because its structure and functions are closely tied to HDL biology and cholesterol transport. Investigations can relate its molecular characteristics and interactions to lipid metabolism and cardiovascular disease research. Its value lies in connecting a measurable protein component with biological processes relevant to cholesterol handling and disease studies.
ApoA-I provides a biological target for strategies designed around HDL function. Because it promotes cholesterol acceptance and activates LCAT, research can examine whether influencing its structure, activity, or interactions affects cholesterol transport. These approaches remain part of HDL-based therapeutic research, where the goal is to use established transport mechanisms to address lipid metabolism and cardiovascular disease.