Evidence map›Paper›PMID 19605502›Full record

ArticleDevelopment (Cambridge, England)2009

Regulation of bone formation and remodeling by G-protein-coupled receptor 48.

Jian Luo, Wei Zhou, Xin Zhou, Dali Li, Jinsheng Weng, Zhengfang Yi, Sung Gook Cho, Chenghai Li, Tingfang Yi, Xiushan Wu and 4 more

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

99 citing papers in PubMed, 179 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. The function of GPCRs in different bone cells.International journal of biological sciences · 2025
    Review
  7. Article
  8. Review
  9. Comprehensive Analysis of Immune Infiltration and Key Genes in Peri-Implantitis Using Bioinformatics and Molecular Biology Approaches.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

39 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 2 countries.

Jian LuoThe Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
Wei Zhou
Xin Zhou
Dali Li
Jinsheng Weng
Zhengfang Yi
Sung Gook Cho
Chenghai Li
Tingfang Yi
Xiushan Wu
Xiao-Ying Li
Benoit de Crombrugghe
Magnus Höök
Mingyao Liu
Texas A&M University System · USEast China Normal University · CNThe University of Texas MD Anderson Cancer Center · USHunan Normal University · CNShanghai Institute of Hematology · CN

Funding

KiSS1 and Its G-Protein Coupled Receptor in MetastasisR01CA106479 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI LIU, MINGYAO · 2005 to 2009
$1.2M
NCI NIH HHS 1R01CA106479
6 · The paper itself

Abstract

G-protein-coupled receptor (GPCR) 48 (Gpr48; Lgr4), a newly discovered member of the glycoprotein hormone receptor subfamily of GPCRs, is an orphan GPCR of unknown function. Using a knockout mouse model, we have characterized the essential roles of Gpr48 in bone formation and remodeling. Deletion of Gpr48 in mice results in a dramatic delay in osteoblast differentiation and mineralization, but not in chondrocyte proliferation and maturation, during embryonic bone formation. Postnatal bone remodeling is also significantly affected in Gpr48(-/-) mice, including the kinetic indices of bone formation rate, bone mineral density and osteoid formation, whereas the activity and number of osteoclasts are increased as assessed by tartrate-resistant acid phosphatase staining. Examination of the molecular mechanism of Gpr48 action in bone formation revealed that Gpr48 can activate the cAMP-PKA-CREB signaling pathway to regulate the expression level of Atf4 in osteoblasts. Furthermore, we show that Gpr48 significantly downregulates the expression levels of Atf4 target genes/proteins, such as osteocalcin (Ocn; Bglap2), bone sialoprotein (Bsp; Ibsp) and collagen. Together, our data demonstrate that Gpr48 regulates bone formation and remodeling through the cAMP-PKA-Atf4 signaling pathway.

Indexed as

Activating Transcription Factor 4AnimalsBone and BonesBone DensityBone RemodelingCell DifferentiationCells, CulturedChondrocytesCollagenCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinEmbryo, MammalianGene Expression Regulation, DevelopmentalIntegrin-Binding SialoproteinMiceActivating Transcription Factor 4Atf4 protein, mouseCollagenCreb1 protein, mouseCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinIbsp protein, mouseIntegrin-Binding SialoproteinLGR4 protein, mouseOsteocalcinProtein IsoformsReceptors, G-Protein-CoupledSialoglycoproteins

Identifiers

PMID19605502
PMCPMC2730404
OpenAlexW2097556510

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.