Evidence map›Paper›PMID 26860366›Full record

ArticleScientific reports2016

The Indispensable Role of Cyclin-Dependent Kinase 1 in Skeletal Development.

Masanori Saito, Mieradili Mulati, S Zakiah A Talib, Philipp Kaldis, Shu Takeda, Atsushi Okawa, Hiroyuki Inose

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  4. p57International journal of molecular sciences · 2024
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  18. Identification of Pivotal Genes and Pathways in Osteoarthritic Degenerative Meniscal Lesions via Bioinformatics Analysis of the GSE52042 Dataset.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  19. 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

7 authors at 3 institutions in 2 countries.

Masanori SaitoDepartment of Orthopedics, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Mieradili MulatiDepartment of Orthopedics, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
S Zakiah A TalibInstitute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology and Research), 61 Biopolis Drive, Proteos#3-09, Singapore 138673, Republic of Singapore.
Philipp KaldisInstitute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology and Research), 61 Biopolis Drive, Proteos#3-09, Singapore 138673, Republic of Singapore.
Shu TakedaDepartment of Physiology and Cell Biology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Atsushi OkawaDepartment of Orthopedics, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Hiroyuki InoseDepartment of Orthopedics, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Tokyo Medical and Dental University · JPAgency for Science, Technology and Research · SGInstitute of Molecular and Cell Biology · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal development is tightly regulated through the processes of chondrocyte proliferation and differentiation. Although the involvement of transcription and growth factors on the regulation of skeletal development has been extensively studied, the role of cell cycle regulatory proteins in this process remains elusive. To date, through cell-specific loss-of-function experiments in vivo, no cell cycle regulatory proteins have yet been conclusively shown to regulate skeletal development. Here, we demonstrate that cyclin-dependent kinase 1 (Cdk1) regulates skeletal development based on chondrocyte-specific loss-of-function experiments performed in a mouse model. Cdk1 is highly expressed in columnar proliferative chondrocytes and is greatly downregulated upon differentiation into hypertrophic chondrocytes. Cdk1 is essential for proper chondrocyte proliferation and deletion of Cdk1 resulted in accelerated differentiation of chondrocytes. In vitro and ex vivo analyses revealed that Cdk1 is an essential cell cycle regulatory protein for parathyroid hormone-related peptide (PTHrP) signaling pathway, which is critical to chondrocyte proliferation and differentiation. These results demonstrate that Cdk1 functions as a molecular switch from proliferation to hypertrophic differentiation of chondrocytes and thus is indispensable for skeletal development. Given the availability of inhibitors of Cdk1 activity, our results could provide insight for the treatment of diseases involving abnormal chondrocyte proliferation, such as osteoarthritis.

Indexed as

Bone DevelopmentAnimalsBlotting, WesternBone and BonesCDC2 Protein KinaseCell DifferentiationCell LineCell ProliferationChondrocytesChondrogenesisCollagen Type IICollagen Type XIn Situ Hybridization, FluorescenceIn Vitro TechniquesMiceMice, KnockoutCDC2 Protein KinaseCollagen Type IICollagen Type XParathyroid Hormone-Related ProteinRNA, Small Interfering

Identifiers

PMID26860366
PMCPMC4816159
OpenAlexW2408841485

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.