Evidence map›Paper›PMID 21917726›Full record

ArticleJournal of lipid research2011

C323 of SR-BI is required for SR-BI-mediated HDL binding and cholesteryl ester uptake.

Ling Guo, Min Chen, Zhiqing Song, Alan Daugherty, Xiang-An Li

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. New developments in selective cholesteryl ester uptake.Current opinion in lipidology · 2013
    Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Ling GuoDepartment of Pediatrics, University of Kentucky Medical School, Lexington, KY.
Min ChenDepartment of Pediatrics, University of Kentucky Medical School, Lexington, KY; Taian Central Hospital, Taian, Shandong, China.
Zhiqing SongDepartment of Pediatrics, University of Kentucky Medical School, Lexington, KY; Taian Central Hospital, Taian, Shandong, China.
Alan DaughertySaha Cardiovascular Research Center, University of Kentucky Medical School, Lexington, KY and.
Xiang-An LiDepartment of Pediatrics, University of Kentucky Medical School, Lexington, KY; Saha Cardiovascular Research Center, University of Kentucky Medical School, Lexington, KY and; Graduate Center for Nutritional Sciences, University of Kentucky Medical School, Lexington, KY; and. Electronic address: xli2@email.uky.edu.
University of Kentucky · US

Funding

Role of SR-BI in LPS detoxificationR01GM085231 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, XIANG-AN · 2008 to 2012
$1.5M
NIGMS NIH HHS R01 GM-085231NIGMS NIH HHS R01 GM085231
6 · The paper itself

Abstract

Scavenger receptor BI (SR-BI) is an HDL receptor. It binds HDL and mediates the uptake of cholesteryl ester from HDL. Early studies have pointed out that the extracellular domain of SR-BI is critical for SR-BI-mediated cholesteryl ester uptake. However, the extracellular loop of SR-BI is large: it contains 403 amino acids. The HDL binding site and the modulation of SR-BI-mediated cholesteryl ester uptake remain to be identified. In this study, using C323G mutant SR-BI, we showed that C323G mutant SR-BI lost its HDL binding and cholesteryl ester uptake activity, indicating that the highly conserved C323 is required for SR-BI-mediated HDL binding and cholesteryl ester uptake. Using a blocking antibody against C323 region, we demonstrated that C323 is directly involved in HDL binding and likely an HDL binding site. Using C323G mutant transgenic mouse model, we further demonstrated that C323 of SR-BI is required for regulating plasma cholesterol levels in vivo. Using redox reagents, we showed that physiological relevant levels of H(2)O(2) upregulated the SR-BI-mediated cholesteryl ester uptake activity by 65%, whereas GSH or DTT significantly downregulated SR-BI-mediated cholesteryl ester uptake activity by 45%. C323 of SR-BI is critical for SR-BI-mediated HDL binding and cholesteryl ester uptake, and changes in redox status may be a regulatory factor modulating SR-BI-mediated cholesterol transport.

Indexed as

CysteineAnimalsCaveolaeCHO CellsCholesterol EstersCricetinaeCricetulusFemaleHumansLipoproteins, HDLMiceOxidation-ReductionProtein BindingProtein TransportScavenger Receptors, Class BCholesterol EstersCysteineLipoproteins, HDLSCARB1 protein, humanScavenger Receptors, Class B

Identifiers

PMID21917726
PMCPMC3220294
OpenAlexW2139656515

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.