Evidence map›Paper›PMID 30902252›Full record

ReviewCurrent topics in developmental biology2019

Roles and regulation of SOX transcription factors in skeletogenesis.

Véronique Lefebvre

Abstract readReview
In one paragraph

Review in Current topics in developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
–field-weighted citation impact
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

76 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Identification of a Force-Induced Sox9Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. Article
  7. Role of the transcription factorTranslational cancer research · 2025
    Article
  8. Review
  9. Review
  10. An inducible mouse model of osteogenesis imperfecta type V reveals aberrant osteogenesis caused by Ifitm5 c.-14C>T mutation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Variants in the SOX9 transactivation middle domain induce axial skeleton dysplasia and scoliosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

16 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

1 author.

Véronique LefebvreThe Children's Hospital of Philadelphia, Philadelphia, PA, United States. Electronic address: lefebvrev1@email.chop.edu.

Funding

Sox9-mediated control of chondrogenesisR01AR046249 · NIAMS · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI LEFEBVRE, VERONIQUE M · 1999 to 2015
$4.9M
Roles of SOX8 and SOX9 in Adult Articular CartilageR01AR072649 · NIAMS · CHILDREN'S HOSP OF PHILADELPHIA · PI LEFEBVRE, VERONIQUE M · 2018 to 2022
$2.9M
Roles of SOXC proteins in osteogenic cellsR01AR068308 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI LEFEBVRE, VERONIQUE M · 2016 to 2020
$2.4M
ROLES OF SOX C GENES IN SKELETOGENESISR01AR054153 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI LEFEBVRE, VERONIQUE M · 2006 to 2010
$1.6M
NIAMS NIH HHS R01 AR046249NIAMS NIH HHS R01 AR054153NIAMS NIH HHS R01 AR068308NIAMS NIH HHS R01 AR072649
6 · The paper itself

Abstract

SOX transcription factors participate in the specification, differentiation and activities of many cell types in development and beyond. The 20 mammalian family members are distributed into eight groups based on sequence identity, and while co-expressed same-group proteins often have redundant functions, different-group proteins typically have distinct functions. More than a handful of SOX proteins have pivotal roles in skeletogenesis. Heterozygous mutations in their genes cause human diseases, in which skeletal dysmorphism is a major feature, such as campomelic dysplasia (SOX9), or a minor feature, such as LAMSHF syndrome (SOX5) and Coffin-Siris-like syndromes (SOX4 and SOX11). Loss- and gain-of-function experiments in animal models have revealed that SOX4 and SOX11 (SOXC group) promote skeletal progenitor survival and control skeleton patterning and growth; SOX8 (SOXE group) delays the differentiation of osteoblast progenitors; SOX9 (SOXE group) is essential for chondrocyte fate maintenance and differentiation, and works in cooperation with SOX5 and SOX6 (SOXD group) and other types of transcription factors. These and other SOX proteins have also been proposed, mainly through in vitro experiments, to have key roles in other aspects of skeletogenesis, such as SOX2 in osteoblast stem cell self-renewal. We here review current knowledge of well-established and proposed skeletogenic roles of SOX proteins, their transcriptional and non-transcriptional actions, and their modes of regulation at the gene, RNA and protein levels. We also discuss gaps in knowledge and directions for future research to further decipher mechanisms underlying skeletogenesis in health and diseases and identify treatment options for skeletal malformation and degeneration diseases.

Indexed as

OsteogenesisAnimalsBone and BonesChondrogenesisGene Expression Regulation, DevelopmentalHumansMutationSOX Transcription FactorsSOX Transcription FactorsCell differentiationCell specificationChondrocyteGene regulationOsteoblastSkeletogenesisSOXTranscriptional regulationTranscription factor

Identifiers

PMID30902252
PMCPMC6955022

What OpenQuestion holds

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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.