Evidence map›Paper›PMID 35461467›Full record

ArticleMedical molecular morphology2022

Induced pluripotent stem cells from homozygous Runx2-deficient mice show poor response to vitamin D during osteoblastic differentiation.

Hideto Aoki, Eiichi Suzuki, Takashi Nakamura, Shoko Onodera, Akiko Saito, Manami Ohtaka, Mahito Nakanishi, Ken Nishimura, Atsushi Saito, Toshifumi Azuma

Abstract read
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In one paragraph

Article in Medical molecular morphology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Downregulation of Nesprin1 by Runx2 deficiency is critical for the development of skeletal laminopathy-like pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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

10 authors at 3 institutions in 1 country.

Hideto AokiDepartment of Periodontology, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Eiichi SuzukiDepartment of Periodontology, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Takashi NakamuraDepartment of Biochemistry, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Shoko OnoderaDepartment of Biochemistry, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Akiko SaitoDepartment of Biochemistry, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.
Manami OhtakaBiotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST), 1-1-1 Umezono, Tsukuba, Ibaraki, 305-8560, Japan.
Mahito NakanishiBiotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST), 1-1-1 Umezono, Tsukuba, Ibaraki, 305-8560, Japan.
Ken NishimuraLaboratory of Gene Regulation, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
Atsushi SaitoDepartment of Periodontology, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan.ORCID http://orcid.org/0000-0002-0065-2207
Toshifumi AzumaDepartment of Biochemistry, Tokyo Dental College, 2-9-18 Kanda-MisakiCho, Chiyoda-ku, Tokyo, 101-0061, Japan. tazuma@tdc.ac.jp.ORCID http://orcid.org/0000-0002-0746-8138
Tokyo Dental College · JPNational Institute of Advanced Industrial Science and Technology · JPUniversity of Tsukuba · JP

Funding

Japan Society for the Promotion of Science 18H03007Japan Society for the Promotion of Science 18K17056Japan Society for the Promotion of Science 26861560
6 · The paper itself

Abstract

Cleidocranial dysplasia (CCD) is a hereditary disorder associated with skeletal dysplasia and dental abnormalities. CCD arises from heterozygous loss of function mutations in the Runt-related transcription factor 2 (RUNX2) gene. Osteoporosis is often observed in CCD patients and conventional vitamin D supplementation is recommended. However, sufficient evidences have not been presented yet. This study investigated the role of RUNX2 in osteoblastic differentiation and sought to identify potential target genes for the treatment of osteoporosis associated with CCD, using induced pluripotent stem cell (iPSC) technology. We successfully established Runx2

Indexed as

Cleidocranial DysplasiaCore Binding Factor Alpha 1 SubunitInduced Pluripotent Stem CellsOsteoporosisVitamin DAnimalsCell DifferentiationMiceMice, KnockoutOsteoblastsCore Binding Factor Alpha 1 SubunitRunx2 protein, mouseVitamin DCleidocranial dysplasiamiPSCsOsteoporosisRanklRunx2Vdr

Identifiers

PMID35461467
OpenAlexW4224242251

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.