ArticlePloS one2012
Functional characterization of newly-discovered mutations in human SR-BI.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
The trial behind it
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
29 citing papers in PubMed, 49 citations in OpenAlex.
- SR-B1's Next Top Model: Structural Perspectives on the Functions of the HDL Receptor.Current atherosclerosis reports · 2022Review
- Article
- HDL and Scavenger Receptor Class B Type I (SRBI).Advances in experimental medicine and biology · 2022Review
- Article
- Hyperalphalipoproteinemia and Beyond: The Role of HDL in Cardiovascular Diseases.Life (Basel, Switzerland) · 2021Review
- SR-B1, a Key Receptor Involved in the Progression of Cardiovascular Disease: A Perspective from Mice and Human Genetic Studies.Biomedicines · 2021Review
- Viral and host heterogeneity and their effects on the viral life cycle.Nature reviews. Microbiology · 2021Review
- Review
- Structure-function analysis of naturally occurring apolipoprotein A-I L144R, A164S and L178P mutants provides insight on their role on HDL levels and cardiovascular risk.Cellular and molecular life sciences : CMLS · 2021Article
- Human variant of scavenger receptor BI (R174C) exhibits impaired cholesterol transport functions.Journal of lipid research · 2021Article
- Reduced CETP glycosylation and activity in patients with homozygous B4GALT1 mutations.Journal of inherited metabolic disease · 2020Article
- Proline residues in scavenger receptor-BI's C-terminal region support efficient cholesterol transport.The Biochemical journal · 2019Article
- Significance of Cholesterol-Binding Motifs in ABCA1, ABCG1, and SR-B1 Structure.The Journal of membrane biology · 2019Article
- SR-BI Interactome Analysis Reveals a Proviral Role for UGGT1 in Hepatitis C Virus Entry.Frontiers in microbiology · 2019Article
- Cholesterol trafficking and raft-like membrane domain composition mediate scavenger receptor class B type 1-dependent lipid sensing in intestinal epithelial cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Intracellular and Plasma Membrane Events in Cholesterol Transport and Homeostasis.Journal of lipids · 2018Review
- SCARB1 variants and HCV infection: Host susceptibility is lost in translation.Journal of hepatology · 2017Article
- Single amino acid mutation of SR-BI decreases infectivity of hepatitis C virus derived from cell culture in a cell culture model.World journal of gastroenterology · 2017Article
- High-density lipoprotein receptor SCARB1 is required for carotenoid coloration in birds.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- NMR Structure of the C-Terminal Transmembrane Domain of the HDL Receptor, SR-BI, and a Functionally Relevant Leucine Zipper Motif.Structure (London, England : 1993) · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In rodents, SR-BI has been firmly established as a physiologically relevant HDL receptor that mediates removal of HDL-cholesteryl esters (CE). However, its role in human lipoprotein metabolism is less defined. Recently, two unique point mutations in human SR-BI - S112F or T175A - were identified in subjects with high HDL-cholesterol (HDL-C) levels. We hypothesized that mutation of these conserved residues would compromise the cholesterol-transport functions of SR-BI. To test this hypothesis, S112F- and T175A-SR-BI were generated by site-directed mutagenesis. Cell surface expression was confirmed for both mutant receptors in COS-7 cells upon transient transfection, albeit at lower levels for T175A-SR-BI. Both mutant receptors displayed defective HDL binding, selective uptake of HDL-CE and release of free cholesterol (FC) from cells to HDL. Mutant receptors were also unable to re-organize plasma membrane pools of FC. While these impaired functions were independent of receptor oligomerization, inability of T175A-SR-BI to mediate cholesterol-transport functions could be related to altered N-linked glycosylation status. In conclusion, high HDL-C levels observed in carriers of S112F- or T175A-SR-BI mutant receptors are consistent with the inability of these SR-BI receptors to mediate efficient selective uptake of HDL-CE, and suggest that increased plasma HDL concentrations in these settings may not be associated with lower risk of cardiovascular disease.
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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.