Evidence map›Paper›PMID 29520264›Full record

ArticleFrontiers in immunology2018

Monomeric C-Reactive Protein Binds and Neutralizes Receptor Activator of NF-κB Ligand-Induced Osteoclast Differentiation.

Zhe-Kun Jia, Hai-Yun Li, Yu-Lin Liang, Lawrence Albert Potempa, Shang-Rong Ji, Yi Wu

Erratum issuedAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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.

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  12. Monomeric C reactive protein (mCRP) regulates inflammatory responses in human and mouse chondrocytes.Laboratory investigation; a journal of technical methods and pathology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Zhe-Kun JiaMOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, China.
Hai-Yun LiMOE Key Laboratory of Environment and Genes Related to Diseases, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.
Yu-Lin LiangMOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, China.
Lawrence Albert PotempaRoosevelt University College of Pharmacy, Schaumburg, IL, United States.
Shang-Rong JiMOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, China.
Yi WuMOE Key Laboratory of Environment and Genes Related to Diseases, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-reactive protein (CRP) is an established marker of rheumatoid arthritis (RA) but with ill-defined actions in the pathogenesis. Here, we show that CRP regulates the differentiation of osteoclasts, a central mediator of joint inflammation and bone erosion in RA, in a conformation- and receptor activator of NF-κB ligand (RANKL)-dependent manner. CRP in the native conformation is ineffective, whereas the monomeric conformation (mCRP) actively modulates osteoclast differentiation through NF-κB and phospholipase C signaling. Moreover, mCRP can bind RANKL, the major driver of osteoclast differentiation, and abrogate its activities. The binding and inhibition of RANKL are mediated by the cholesterol binding sequence (CBS) of mCRP. Corroborating the

Indexed as

AnimalsArthritis, RheumatoidCell DifferentiationC-Reactive ProteinDisease Models, AnimalHumansLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutOsteoclastsOsteolysisPrimary Cell CultureProtein ConformationProtein Interaction Domains and MotifsC-Reactive ProteinLipopolysaccharidesRANK LigandTnfsf11 protein, mouseC-reactive proteininflammationosteoclastreceptor activator of NF-κB ligandrheumatoid arthritis

Identifiers

PMID29520264
PMCPMC5827540

What OpenQuestion holds

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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.