ArticleArteriosclerosis, thrombosis, and vascular biology2013
ABCA1 mediates unfolding of apolipoprotein AI N terminus on the cell surface before lipidation and release of nascent high-density lipoprotein.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- ABCA1-Mediated Structural Diversity of HDL Subspecies and Their Proposed Roles in Cardioprotection.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- 3-Hydroxystearic acid promotes cholesterol efflux and attenuates atherosclerosis via the ALKBH5/PAX-8/ABCA1 pathway.Frontiers in immunology · 2026Article
- Treatment Resistant Persister Cells Exploit Macrophage Lipid Metabolism to Sustain Glioblastoma Growth.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic crossroads in metabolic and cardiovascular health: the role of DNA methylation in type 2 diabetes and cardiovascular diseases.Cardiovascular diabetology · 2025Review
- Reverse cholesterol transport: current assay methods, alterations with disease and response to therapeutic intervention.Frontiers in cardiovascular medicine · 2025Review
- Is reverse cholesterol transport regulated by active cholesterol?Journal of lipid research · 2023Review
- Activity and Structural Dynamics of Human ABCA1 in a Lipid Membrane.Journal of molecular biology · 2023Article
- Development and validation of novel automatable assay for cholesterol efflux capacity.Bioscience reports · 2023Article
- Review
- Crosstalk Between Cholesterol, ABC Transporters, and PIP2 in Inflammation and Atherosclerosis.Advances in experimental medicine and biology · 2023Article
- Molecular mechanisms for ABCA1-mediated cholesterol efflux.Cell cycle (Georgetown, Tex.) · 2022Review
- HDL Is Not Dead Yet.Biomedicines · 2022Review
- Gasdermin D Mediates Inflammation-Induced Defects in Reverse Cholesterol Transport and Promotes Atherosclerosis.Frontiers in cell and developmental biology · 2021Article
- New Horizons for the Roles and Association of APE1/Ref-1 and ABCA1 in Atherosclerosis.Journal of inflammation research · 2021Review
- The crosstalk of ABCA1 and ANXA1: a potential mechanism for protection against atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2020Review
- Article
- A Novel Cell-Free Fluorescent Assay for HDL Function: Low Apolipoprotein A1 Exchange Rate Associated with Increased Incident Cardiovascular Events.The journal of applied laboratory medicine · 2020Article
- Mechanisms and regulation of cholesterol homeostasis.Nature reviews. Molecular cell biology · 2020Review
- First eight residues of apolipoprotein A-I mediate the C-terminus control of helical bundle unfolding and its lipidation.PloS one · 2020Article
- Assessment of HDL Cholesterol Removal Capacity: Toward Clinical Application.Journal of atherosclerosis and thrombosis · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo gain insight into the mechanism by which ABCA1 generates nascent high-density lipoprotein. APPROACH AND
resultsHEK293 cells were stably transfected with ABCA1 vectors, encoding wild type, and the W590S and C1477R Tangier disease mutation isoforms, along with the K939M ATP-binding domain mutant. Apolipoprotein AI (ApoAI) binding, plasma membrane remodeling, cholesterol efflux, apoAI cell surface unfolding, and apoAI cell surface lipidation were determined, the latter 2 measured using novel fluorescent apoAI indicators. The W590S isoform had decreased plasma membrane remodeling and lipid efflux activities, and the C1477R isoform had decreased apoAI binding, and lipid efflux activities, whereas the K939M isoform did not bind apoAI, remodel the membrane, or efflux cholesterol. However, all ABCA1 isoforms led to apoAI unfolding at the cell surface, which was higher for the isoforms that increased apoAI binding. ApoAI lipidation was not detected on ABCA1-expressing cells, only in the conditioned medium, consistent with rapid release of nascent high-density lipoprotein from ABCA1-expressing cells.
conclusionsWe identified a third activity of ABCA1, the ability to unfold the N terminus of apoAI on the cell surface. Our results support a model in which unfolded apoAI on the cell surface is an intermediate in its lipidation and that, once apoAI is lipidated, it forms an unstable structure that is rapidly released from the cells to generate high-density lipoprotein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.