Evidence map›Paper›PMID 11585922›Full record

ArticleMolecular and cellular biology2001

Common regulation of growth arrest and differentiation of osteoblasts by helix-loop-helix factors.

N Funato, K Ohtani, K Ohyama, T Kuroda, M Nakamura

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  17. E proteins regulate osteoclast maturation and survival.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012
    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

5 authors at 2 institutions in 2 countries.

N FunatoHuman Gene Sciences Center, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.
K Ohtani
K Ohyama
T Kuroda
M Nakamura
Tokyo Medical and Dental University · JPCenter for Human Genetics · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular differentiation entails the coordination of cell cycle arrest and tissue-specific gene expression. We investigated the involvement of basic helix-loop-helix (bHLH) factors in differentiation of osteoblasts using the human osteoblastic cell line MG63. Serum starvation induced growth arrest at G1 phase, accompanied by expression of cyclin-dependent kinase inhibitor p21(WAF1/Cip1). Reporter assays with the p21 gene promoter demonstrated that the combination of E2A (E12 or E47) and coactivator CBP was responsible for p21 induction independent of p53. Twist inhibited E2A-CBP-dependent activation of the exogenous and endogenous p21 promoters. Ids similarly inhibited the exogenously transfected p21 promoter; however less antagonistic effect on the endogenous p21 promoter was observed. Twist was predominantly present in nuclei in MG63 cells growing in complete medium, while it localized mainly in the cytoplasm after serum starvation. The fibroblast growth factor receptor 3 gene (FGFR3), which generates signals leading to differentiation of osteoblasts, was found to be controlled by the same transcriptional regulation as the p21 gene. E2A and Twist influenced alkaline phosphatase expression, a consensus marker of osteoblast differentiation. Expression of E2A and FGFR3 was seen at the location of osteoblast differentiation in the calvaria of mouse embryos, implicating bHLH molecules in physiological osteoblast differentiation. These results demonstrate that a common regulatory system is involved in at least two distinct steps in osteoblastic differentiation. Our results also provide the molecular basis of Saethre-Chotzen syndrome, caused by mutations of the TWIST and FGFR3 genes.

Indexed as

Helix-Loop-Helix MotifsProtein-Tyrosine KinasesAlkaline PhosphataseBasic Helix-Loop-Helix ProteinsBlotting, WesternBromodeoxyuridineCell DifferentiationCell DivisionCell LineCulture Media, Serum-FreeCyclin-Dependent Kinase Inhibitor p21CyclinsCytoplasmDNA-Binding ProteinsG1 PhaseGenes, ReporterAlkaline PhosphataseBasic Helix-Loop-Helix ProteinsBromodeoxyuridineCDKN1A protein, humanCulture Media, Serum-FreeCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsFGFR3 protein, humanNuclear ProteinsProtein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 3Receptors, Fibroblast Growth FactorTranscription FactorsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID11585922
PMCPMC99914
OpenAlexW2102670644

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.