Evidence map›Paper›PMID 25746793›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Mesenchyme-specific overexpression of nucleolar protein 66 in mice inhibits skeletal growth and bone formation.

Qin Chen, Liping Zhang, Benoit de Crombrugghe, Ralf Krahe

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Mechanisms Regulating Muscle Protein Synthesis in CKD.Journal of the American Society of Nephrology : JASN · 2020
    Article
  6. The small members of the JMJD protein family: Enzymatic jewels or jinxes?Biochimica et biophysica acta. Reviews on cancer · 2019
    Review
  7. Review
  8. 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

4 authors at 2 institutions in 1 country.

Qin Chen*Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas, USA; and Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA qchen1@mdanderson.org.
Liping Zhang*Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas, USA; and Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Benoit de Crombrugghe*Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas, USA; and Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Ralf Krahe*Department of Genetics, University of Texas MD Anderson Cancer Center, Houston, Texas, USA; and Nephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
Genetic Control of Osteoblast DifferentiationR01AR049072 · NIAMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DE CROMBRUGGHE, BENOIT · 2002 to 2018
$5.9M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NIAMS NIH HHS R01 AR049072NIAMS NIH HHS R01 AR49072NIDDK NIH HHS P30 DK079638NIDDK NIH HHS P30-DK079638)
6 · The paper itself

Abstract

Previous studies showed that nucleolar protein 66 (NO66), the Jumonji C-domain-containing histone demethylase for methylated histone H3K4 and H3K36 (H3K36me), negatively regulates osteoblast differentiation in vitro by inhibiting the activity of transcription factor osterix (Osx). However, whether NO66 affects mammalian skeletogenesis in vivo is not yet known. Here, we generated transgenic (TG) mice overexpressing a flag-tagged NO66 transgene driven by the Prx1 (paired related homeobox 1) promoter. We found that NO66 overexpression in Prx1-expressing mesenchymal cells inhibited skeletal growth and bone formation. The inhibitory phenotype was associated with >50% decreases in chondrocyte/osteoblast proliferation and differentiation. Moreover, we found that in bones of NO66-TG mice, expression of Igf1, Igf1 receptor (Igf1r), runt-related transcription factor 2, and Osx was significantly down-regulated (P < 0.05). Consistent with these results, we observed >50% reduction in levels of phosphorylated protein kinase B (Akt) and H3K36me3 in bones of NO66-TG mice, suggesting an inverse correlation between NO66 histone demethylase and the activity of IGF1R/Akt signaling. This correlation was further confirmed by in vitro assays of C2C12 cells with NO66 overexpression. We propose that the decrease in the IGF1R/Akt signaling pathway in mice with mesenchymal overexpression of NO66 may contribute in part to the inhibition of skeletal growth and bone formation.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBlotting, WesternBone and BonesCell DifferentiationCell LineCell ProliferationChondrocytesImmunohistochemistryInsulin-Like Growth Factor IJumonji Domain-Containing Histone DemethylasesMesodermMice, TransgenicMicroscopy, FluorescenceOsteoblastsOsteogenesisinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IJumonji Domain-Containing Histone Demethylasesnucleolar protein 66, mouseProto-Oncogene Proteins c-aktReceptor, IGF Type 1Sp7 protein, mouseSp7 Transcription FactorTranscription Factorshistone demethylaseIGF1R/Akt signaling pathwayosterixtransgenic mice

Identifiers

PMID25746793
PMCPMC4447221
OpenAlexW2083857228

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.