Evidence map›Paper›PMID 22351765›Full record

ArticleThe Journal of biological chemistry2012

Neural crest deletion of Dlx3 leads to major dentin defects through down-regulation of Dspp.

Olivier Duverger, Angela Zah, Juliane Isaac, Hong-Wei Sun, Anne K Bartels, Jane B Lian, Ariane Berdal, Joonsung Hwang, Maria I Morasso

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Article
  3. Genes & diseases · 2026
    Article
  4. Review
  5. Article
  6. METTL3-mediated pre-miR-665/DLX3 mExperimental & molecular medicine · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Trafficking and secretion of keratin 75 by ameloblastsThe Journal of biological chemistry · 2019
    Article
  18. Article
  19. Article
  20. 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

9 authors at 5 institutions in 3 countries.

Olivier DuvergerDevelopmental Skin Biology Section, NIAMS, National Institutes of Health, Bethesda, Maryland 20892, USA.
Angela Zah
Juliane Isaac
Hong-Wei Sun
Anne K Bartels
Jane B Lian
Ariane Berdal
Joonsung Hwang
Maria I Morasso
Skin Research Center · FRNational Institutes of Health · USInserm · FRSKiN Health · CAUniversity of Massachusetts Chan Medical School · US

Funding

NIAMS Light Imaging FacilityZICAR041186 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RANDAZZO, DAVIDE · 2010 to 2025
$18.2M
Applying Bioinformatics to Research in Immune, Muscle, and Bone DiseasesZIHAR041173 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GADINA, MASSIMO · 2009 to 2020
$11.0M
Ectodermal Dysplasias and Regulation of Ectodermal Appendage DevelopmentZIAAR041171 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MORASSO, MARIA · 2009 to 2024
$10.8M
Synthesis of Osteocalcin in BoneR37DE012528 · NIDCR · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B. · 2008 to 2017
$5.0M
Intramural NIH HHSNIDCR NIH HHS R37 DE012528
6 · The paper itself

Abstract

During development, Dlx3 is expressed in ectodermal appendages such as hair and teeth. Thus far, the evidence that Dlx3 plays a crucial role in tooth development comes from reports showing that autosomal dominant mutations in DLX3 result in severe enamel and dentin defects leading to abscesses and infections. However, the normal function of DLX3 in odontogenesis remains unknown. Here, we use a mouse model to demonstrate that the absence of Dlx3 in the neural crest results in major impairment of odontoblast differentiation and dentin production. Mutant mice develop brittle teeth with hypoplastic dentin and molars with an enlarged pulp chamber and underdeveloped roots. Using this mouse model, we found that dentin sialophosphoprotein (Dspp), a major component of the dentin matrix, is strongly down-regulated in odontoblasts lacking Dlx3. Using ChIP-seq, we further demonstrate the direct binding of Dlx3 to the Dspp promoter in vivo. Luciferase reporter assays determined that Dlx3 positively regulates Dspp expression. This establishes a regulatory pathway where the transcription factor Dlx3 is essential in dentin formation by directly regulating a crucial matrix protein.

Indexed as

Gene DeletionGene Expression Regulation, DevelopmentalAmeloblastsAnimalsBase SequenceCell DifferentiationCell LineDental EnamelDentinDentin DysplasiaDentin SialophosphoproteinDown-RegulationExtracellular Matrix ProteinsGenes, ReporterHomeodomain ProteinsLuciferases, RenillaDentin SialophosphoproteinDistal-less homeobox proteinsExtracellular Matrix ProteinsHomeodomain ProteinsLuciferases, RenillaPhosphoproteinsSialoglycoproteinsTranscription Factors

Identifiers

PMID22351765
PMCPMC3320974
OpenAlexW1968528634

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.