Evidence map›Paper›PMID 23589304›Full record

ArticleThe Journal of biological chemistry2013

Lgr4/Gpr48 negatively regulates TLR2/4-associated pattern recognition and innate immunity by targeting CD14 expression.

Bing Du, Weijia Luo, Ruimei Li, Binghe Tan, Honghui Han, Xiaoling Lu, Dali Li, Min Qian, Dekai Zhang, Yongxiang Zhao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. The Role of LGR4 (GPR48) in Normal and Cancer Processes.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Review
  9. Enhanced Expression of miR-34a EnhancesOxidative medicine and cellular longevity · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. LGR4 modulates breast cancer initiation, metastasis, and cancer stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

11 authors at 4 institutions in 2 countries.

Bing DuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.
Weijia Luo
Ruimei Li
Binghe Tan
Honghui Han
Xiaoling Lu
Dali Li
Min Qian
Dekai Zhang
Yongxiang Zhao
Mingyao Liu
East China Normal University · CNGuangxi Medical University · CNTexas A&M Health Science Center · USTexas A&M University · US

Funding

Targeting the prostate-specific G-protein coupled receptors in prostate tumorR01CA134731 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI LIU, MINGYAO · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA134731NCI NIH HHS R01CA134731
6 · The paper itself

Abstract

The recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs) is pivotal in both innate and adaptive immune responses. Here we demonstrate that deletion of Lgr4/Gpr48 (G-protein-coupled receptor 48), a seven-transmembrane glycoprotein hormone receptor, potentiates TLR2/4-associated cytokine production and attenuates mouse resistance to septic shock. The expression of CD14, a co-receptor for TLR2/4-associated pathogen-associated molecular patterns, is increased significantly in Lgr4-deficient macrophages, which is consistent with the increased immune response, whereas the binding activity of cAMP-response element-binding protein is decreased significantly in Lgr4-deficient macrophages, which up-regulate the expression of CD14 at the transcriptional level. Together, our data demonstrate that Lgr4/Gpr48 plays a critical role in modulating the TLR2/4 signaling pathway and represents a useful therapeutic approach of targeting Lgr4/Gpr48 in TLR2/4-associated septic shock and autoimmune diseases.

Indexed as

AnimalsAutoimmune DiseasesCell LineHumansImmunity, InnateLipopolysaccharide ReceptorsMacrophagesMiceMice, KnockoutReceptors, G-Protein-CoupledShock, SepticSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Up-RegulationLGR4 protein, humanLGR4 protein, mouseLipopolysaccharide ReceptorsReceptors, G-Protein-CoupledTLR2 protein, humanTlr2 protein, mouseTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4CD14CREBG-protein-coupled Receptors (GPCRs)Lgr4Pathogen-associated Molecular Pattern (PAMP)SepsisToll-like Receptors (TLR)

Identifiers

PMID23589304
PMCPMC3663533
OpenAlexW1977466146

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.