Evidence map›Paper›PMID 29047264›Full record

ArticleMolecules and cells2017

The Inactivation of ERK1/2, p38 and NF-kB Is Involved in the Down-Regulation of Osteoclastogenesis and Function by A2B Adenosine Receptor Stimulation.

Bo Hyun Kim, Ju Hee Oh, Na Kyung Lee

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  9. Article
  10. Article
  11. Review
  12. The Adenosine ACells · 2019
    Article
  13. Review
  14. Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology.International journal of molecular sciences · 2018
    Review
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

3 authors at 1 institution in 1 country.

Bo Hyun KimDepartment of Medical Science, College of Medical Sciences, Soonchunhyang University, Asan 336-745, Korea.
Ju Hee OhDepartment of Medical Science, College of Medical Sciences, Soonchunhyang University, Asan 336-745, Korea.
Na Kyung LeeDepartment of Medical Science, College of Medical Sciences, Soonchunhyang University, Asan 336-745, Korea.
Soonchunhyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A2B adenosine receptor (A2BAR) is known to be the regulator of bone homeostasis, but its regulatory mechanisms in osteoclast formation are less well-defined. Here, we demonstrate the effect of A2BAR stimulation on osteoclast differentiation and activity by RANKL. A2BAR was expressed in bone marrow-derived monocyte/macrophage (BMM) and RANKL increased A2BAR expression during osteoclastogenesis. A2BAR stimulation with its specific agonist BAY 60-6583 was sufficient to inhibit the activation of ERK1/2, p38 MAP kinases and NF-κB by RANKL as well as it abrogated cell-cell fusion in the late stage of osteoclast differentiation. Stimulation of A2BAR suppressed the expression of osteoclast marker genes, such as

Indexed as

AnimalsBone ResorptionCell DifferentiationGene Expression Regulation, DevelopmentalMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NFATC Transcription FactorsNF-kappa BOsteoclastsOsteogenesisp38 Mitogen-Activated Protein KinasesRANK LigandReceptor, Adenosine A2BSignal TransductionMapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NFATC Transcription FactorsNF-kappa Bp38 Mitogen-Activated Protein KinasesRANK LigandReceptor, Adenosine A2BTnfsf11 protein, mouseA2B adenosine receptorosteoclastogenesisRANKL

Identifiers

PMID29047264
PMCPMC5682252
OpenAlexW2924284801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.