ArticleFrontiers in molecular biosciences2025
A dual-reporter LDLR system integrating fluorescence and luminescence for understanding LDLR regulation and facilitating drug discovery.
Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Modulation of Hepatic Cholesterol-Related Pathways byMolecules (Basel, Switzerland) · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The low-density lipoprotein receptor (LDLR) is integral to cholesterol metabolism and cardiovascular health. Enhancing LDLR expression is a promising strategy for treating hyperlipidemia and reducing the risk of atherosclerosis. However, current LDLR reporter systems have limitations in detecting both transcriptional and translational regulation. To address this, we developed a novel dual-reporter LDLR system incorporating Enhanced Green Fluorescent Protein (EGFP) and Gaussia luciferase (Gluc) to enable precise monitoring of LDLR expression and function. Methods: A CRISPR/Cas9-mediated knock-in strategy was used to integrate EGFP and Gluc upstream of the stop codon located in exon 18 of the LDLR gene in HEK293 cells. The dual-reporter system allows real-time visualization of LDLR expression via EGFP fluorescence and quantitative assessment through secreted Gluc activity. The system was validated using western blotting, immunofluorescence, and functional assays, including DiI-LDL uptake and drug response analyses with statins and PCSK9 inhibitors. Results: The established LDLR-EGFP-Gluc knock-in cell line faithfully recapitulates endogenous LDLR expression and function. EGFP fluorescence accurately reflects LDLR expression dynamics, while Gluc activity provides a highly sensitive and quantitative readout. Functional assays confirmed that LDLR expression responds appropriately to statins and PCSK9 inhibitors. Additionally, screening for transcriptional regulators identified FOXP3 and CREB as novel modulators of LDLR expression, with CREB-mediated regulation involving the sterol regulatory element-binding protein 2 (SREBP2) pathway. Discussion: This dual-reporter system enables complementary monitoring of LDLR dynamics, providing enhanced sensitivity, accuracy, and versatility for studying LDLR regulation and function, as well as facilitating drug discovery targeting hyperlipidemia and cardiovascular diseases.
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Registered trials
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