ArticleInternational journal of molecular sciences2023
MP Allosterically Activates AMPK to Enhance ABCA1 Stability by Retarding the Calpain-Mediated Degradation Pathway.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Mechanisms and therapeutic potential of AMPK signaling pathway in the regulation of lipid metabolism.Molecular biology reports · 2026Review
- Colchicine enhances macrophage cholesterol efflux by targeting DTL-mediated ubiquitination and degradation of ABCA1.RMD open · 2026Article
- Decoding the crosstalk: interplay between macrophage programmed cell death networks and cholesterol efflux.Frontiers in cardiovascular medicine · 2026Review
- Research Status and Latest Progress in the Regulatory Mechanisms of ABCA1.International journal of molecular sciences · 2025Review
- Recent progress of endoplasmic reticulum stress in the mechanism of atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
It is widely recognized that macrophage cholesterol efflux mediated by the ATP-binding cassette transporter A1 (ABCA1) constitutes the initial and rate-limiting step of reverse cholesterol transport (RCT), displaying a negative correlation with the development of atherosclerosis. Although the transcriptional regulation of ABCA1 has been extensively studied in previous research, the impact of post-translational regulation on its expression remains to be elucidated. In this study, we report an AMP-activated protein kinase (AMPK) agonist called ((2R,3S,4R,5R)-3,4-dihydroxy-5-(6-((3-hydroxyphenyl) amino)-9H-purin-9-yl) tetrahydrofuran-2-yl) methyl dihydrogen phosphate (MP), which enhances ABCA1 expression through post-translational regulation rather than transcriptional regulation. By integrating the findings of multiple experiments, it is confirmed that MP directly binds to AMPK with a moderate binding affinity, subsequently triggering its allosteric activation. Further investigations conducted on macrophages unveil a novel mechanism through which MP modulates ABCA1 expression. Specifically, MP downregulates the Cav1.2 channel to obstruct the influx of extracellular Ca
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Registered trials
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