Evidence map›Paper›PMID 20628571›Full record

ArticlePLoS genetics2010

Id4, a new candidate gene for senile osteoporosis, acts as a molecular switch promoting osteoblast differentiation.

Yoshimi Tokuzawa, Ken Yagi, Yzumi Yamashita, Yutaka Nakachi, Itoshi Nikaido, Hidemasa Bono, Yuichi Ninomiya, Yukiko Kanesaki-Yatsuka, Masumi Akita, Hiromi Motegi and 11 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Skeletal Class III Malocclusion Is Associated withInternational journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Deciphering GRINA/Lifeguard1: Nuclear Location, CaInternational journal of molecular sciences · 2019
    Review
  20. Medical Treatment for Osteoporosis: From Molecular to Clinical Opinions.International journal of molecular sciences · 2019
    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

21 authors at 4 institutions in 3 countries.

Yoshimi TokuzawaDivision of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, Hidaka, Saitama, Japan.
Ken Yagi
Yzumi Yamashita
Yutaka Nakachi
Itoshi Nikaido
Hidemasa Bono
Yuichi Ninomiya
Yukiko Kanesaki-Yatsuka
Masumi Akita
Hiromi Motegi
Shigeharu Wakana
Tetsuo Noda
Fred Sablitzky
Shigeki Arai
Riki Kurokawa
Toru Fukuda
Takenobu Katagiri
Christian Schönbach
Tatsuo Suda
Yosuke Mizuno
Yasushi Okazaki
Saitama Medical University · JPRIKEN BioResource Research Center · JPKyushu Institute of Technology · JPUniversity of Nottingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive accumulation of bone marrow adipocytes observed in senile osteoporosis or age-related osteopenia is caused by the unbalanced differentiation of MSCs into bone marrow adipocytes or osteoblasts. Several transcription factors are known to regulate the balance between adipocyte and osteoblast differentiation. However, the molecular mechanisms that regulate the balance between adipocyte and osteoblast differentiation in the bone marrow have yet to be elucidated. To identify candidate genes associated with senile osteoporosis, we performed genome-wide expression analyses of differentiating osteoblasts and adipocytes. Among transcription factors that were enriched in the early phase of differentiation, Id4 was identified as a key molecule affecting the differentiation of both cell types. Experiments using bone marrow-derived stromal cell line ST2 and Id4-deficient mice showed that lack of Id4 drastically reduces osteoblast differentiation and drives differentiation toward adipocytes. On the other hand knockdown of Id4 in adipogenic-induced ST2 cells increased the expression of Ppargamma2, a master regulator of adipocyte differentiation. Similar results were observed in bone marrow cells of femur and tibia of Id4-deficient mice. However the effect of Id4 on Ppargamma2 and adipocyte differentiation is unlikely to be of direct nature. The mechanism of Id4 promoting osteoblast differentiation is associated with the Id4-mediated release of Hes1 from Hes1-Hey2 complexes. Hes1 increases the stability and transcriptional activity of Runx2, a key molecule of osteoblast differentiation, which results in an enhanced osteoblast-specific gene expression. The new role of Id4 in promoting osteoblast differentiation renders it a target for preventing the onset of senile osteoporosis.

Indexed as

Cell DifferentiationAnimalsBasic Helix-Loop-Helix ProteinsCore Binding Factor Alpha 1 SubunitHomeodomain ProteinsInhibitor of Differentiation ProteinsMiceMice, KnockoutOsteoblastsOsteoporosisTranscription Factor HES-1Transcription FactorsUp-RegulationBasic Helix-Loop-Helix ProteinsCore Binding Factor Alpha 1 SubunitHes1 protein, mouseHomeodomain ProteinsIdb4 protein, mouseInhibitor of Differentiation ProteinsRunx2 protein, mouseTranscription Factor HES-1Transcription Factors

Identifiers

PMID20628571
PMCPMC2900302
OpenAlexW2089290843

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.