Evidence map›Paper›PMID 23225263›Full record

ReviewJournal of cellular biochemistry2013

Genetic and molecular control of osterix in skeletal formation.

Krishna M Sinha, Xin Zhou

Abstract readReview
In one paragraph

Review in Journal of cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 291 citations in OpenAlex.

  1. Pooled it
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  7. Dissecting the effects ofActa pharmaceutica Sinica. B · 2025
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96 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Krishna M SinhaDepartment of Endocrine Neoplasia and Hormonal Disorders, UT MD Anderson Cancer Center, Houston, TX 77030, USA. ksinha@mdanderson.org
Xin Zhou
The University of Texas MD Anderson Cancer Center · US

Funding

Genetic Control of Osteoblast DifferentiationR01AR049072 · NIAMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DE CROMBRUGGHE, BENOIT · 2002 to 2018
$5.9M
Epigenetic Control of Osteoblast Differentiation and Bone FormationR03AR061590 · NIAMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SINHA, KRISHNA M · 2011 to 2013
$233k
NIAMS NIH HHS AR049072NIAMS NIH HHS AR061590NIAMS NIH HHS R01 AR049072NIAMS NIH HHS R03 AR061590
6 · The paper itself

Abstract

Osteoblast differentiation is a multi-step process where mesenchymal cells differentiate into osteoblast lineage cells including osteocytes. Osterix (Osx) is an osteoblast-specific transcription factor which activates a repertoire of genes during differentiation of preosteoblasts into mature osteoblasts and osteocytes. The essential role of Osx in the genetic program of bone formation and in bone homeostasis is well established. Osx mutant embryos do not form bone and fail to express osteoblast-specific marker genes. Inactivation of Osx in mice after birth causes multiple skeletal phenotypes including lack of new bone formation, absence of resorption of mineralized cartilage, and defects in osteocyte maturation and function. Since Osx is a major effector in skeletal formation, studies on Osx gained momentum over the last 5-7 years and implicated its important function in tooth formation as well as in healing of bone fractures. This review outlines mouse genetic studies that establish the essential role of Osx in bone and tooth formation as well as in healing of bone fractures. We also discuss the recent advances in regulation of Osx expression, which is under control of a transcriptional network, signaling pathways, and epigenetic regulation. Finally, we summarize important findings on the positive and negative regulation of Osx's transcriptional activity through protein-protein interactions in expression of its target genes during osteoblast differentiation. In particular, the identification of the histone demethylase NO66 as an Osx-interacting protein, which negatively regulates Osx activity opens further avenues in studying epigenetic control of Osx target genes during differentiation and maturation of osteoblasts.

Indexed as

AnimalsBone DiseasesCore Binding Factor Alpha 1 SubunitHumansMutationOdontoblastsOsteogenesisTranscription FactorsCore Binding Factor Alpha 1 SubunitTranscription Factors

Identifiers

PMID23225263
PMCPMC3725781
OpenAlexW2035462789

What OpenQuestion holds

Textmetadata
LicenceTDM
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.