Evidence map›Paper›PMID 27879318›Full record

ArticleThe Journal of biological chemistry2017

Inactivation of Regulatory-associated Protein of mTOR (Raptor)/Mammalian Target of Rapamycin Complex 1 (mTORC1) Signaling in Osteoclasts Increases Bone Mass by Inhibiting Osteoclast Differentiation in Mice.

Qinggang Dai, Furong Xie, Yujiao Han, Xuhui Ma, Siru Zhou, Lingyong Jiang, Weiguo Zou, Jun Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 83 citations in OpenAlex.

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  17. The crosstalk between MYC and mTORC1 during osteoclastogenesis.Frontiers in cell and developmental biology · 2022
    Article
  18. Skeletal diseases caused by mutations inFrontiers in cell and developmental biology · 2022
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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

8 authors at 4 institutions in 2 countries.

Qinggang DaiFrom the Departments of Pediatric Dentistry.
Furong XieFrom the Departments of Pediatric Dentistry.
Yujiao Hanthe State Key Laboratory of Cell Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xuhui MaOral and Maxillofacial Head and Neck Oncology, and.
Siru ZhouCenter of Craniofacial Orthodontics, Department of Oral and Craniomaxillofacial Science, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011 and.
Lingyong JiangCenter of Craniofacial Orthodontics, Department of Oral and Craniomaxillofacial Science, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011 and jly117@sina.com.
Weiguo Zouthe State Key Laboratory of Cell Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China zouwg94@sibcb.ac.cn.
Jun WangFrom the Departments of Pediatric Dentistry, wangjun202@126.com.
Shanghai Jiao Tong University · CNCenter for Excellence in Molecular Cell Science · CNShanghai Ninth People's Hospital · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian target of rapamycin complex 1 (mTORC1) is involved in anabolic metabolism in both osteoblasts and chondrocytes, but the role of mTORC1 in osteoclast biology in vivo remains to be elucidated. In this study, we showed that deletion of regulatory-associated protein of mTOR (Raptor) in osteoclasts led to an increase in bone mass with decreased bone resorption. Raptor-deficient bone marrow-derived macrophages exhibited lower mTORC1-S6K1 signaling and retarded osteoclast differentiation, as determined by the number of osteoclasts, tartrate-resistant acid phosphatase activity, and expression of osteoclast-specific genes. Enforced expression of constitutively active S6K1 rescued the impaired osteoclast differentiation in Raptor-deficient bone marrow-derived macrophages. Furthermore, pharmacological inhibition of mTORC1 signaling by rapamycin could also inhibit osteoclast differentiation and osteoclast-specific gene expression. Taken together, our findings demonstrate that mTORC1 plays a key role in the network of catabolic bone resorption in osteoclasts and may serve as a potential pharmacological target for the regulation of osteoclast activity in bone metabolic disorders.

Indexed as

Cell DifferentiationAdaptor Proteins, Signal TransducingAnimalsBone and BonesBone DensityCells, CulturedMacrophagesMaleMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMultiprotein ComplexesOsteoclastsOsteogenesisPhosphorylationRegulatory-Associated Protein of mTORAdaptor Proteins, Signal TransducingMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesRegulatory-Associated Protein of mTORRptor protein, mouseTOR Serine-Threonine Kinasesbonecell differentiationmTOR complex (mTORC)osteoclastosteoporosisS6 kinase

Identifiers

PMID27879318
PMCPMC5217679
OpenAlexW2555889287

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.