ArticleDevelopmental biology2009
In vivo impact of a 4 bp deletion mutation in the DLX3 gene on bone development.
Article in Developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
The trial behind it
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Suppression of distal-less homeobox 3 increased alveolar bone mass in mouse tooth socket by targeting thrombospondin 1.Journal of dental sciences · 2026Article
- Review
- Review
- MutantPeerJ · 2020Article
- Novel DLX3 variants in amelogenesis imperfecta with attenuated tricho-dento-osseous syndrome.Oral diseases · 2019Article
- Article
- Senescence: novel insight into DLX3 mutations leading to enhanced bone formation in Tricho-Dento-Osseous syndrome.Scientific reports · 2016Article
- Estrogen Receptor α Regulates Dlx3-Mediated Osteoblast Differentiation.Molecules and cells · 2016Article
- MicroRNA 665 Regulates Dentinogenesis through MicroRNA-Mediated Silencing and Epigenetic Mechanisms.Molecular and cellular biology · 2015Article
- DLX3 regulates bone mass by targeting genes supporting osteoblast differentiation and mineral homeostasis in vivo.Cell death and differentiation · 2014Article
- RANK, RANKL and OPG expressions in a permanent molar with a replacement resorption.Odontology · 2013Article
- In vivo impact of Dlx3 conditional inactivation in neural crest-derived craniofacial bones.Journal of cellular physiology · 2013Article
- Neural crest deletion of Dlx3 leads to major dentin defects through down-regulation of Dspp.The Journal of biological chemistry · 2012Article
- Tricho-dento-osseous syndrome: diagnosis and dental management.International journal of dentistry · 2012Article
- Mutant DLX 3 disrupts odontoblast polarization and dentin formation.Developmental biology · 2010Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Distal-less 3 (DLX3) gene mutations are etiologic for Tricho-Dento-Osseous syndrome. To investigate the in vivo impact of mutant DLX3 on bone development, we established transgenic (TG) mice expressing the c.571_574delGGGG DLX-3 gene mutation (MT-DLX3) driven by a mouse 2.3 Col1A1 promoter. Microcomputed tomographic analyses demonstrated markedly increased trabecular bone volume and bone mineral density in femora from TG mice. In ex vivo experiments, TG mice showed enhanced differentiation of bone marrow stromal cells to osteoblasts and increased expression levels of bone formation markers. However, TG mice did not show enhanced dynamic bone formation rates in in vivo fluorochrome double labeling experiments. Osteoclastic differentiation capacities of bone marrow monocytes were reduced in TG mice in the presence of osteoclastogenic factors and the numbers of TRAP(+) osteoclasts on distal metaphyseal trabecular bone surfaces were significantly decreased. TRACP 5b and CTX serum levels were significantly decreased in TG mice, while IFN-gamma levels were significantly increased. These data demonstrate that increased levels of IFN-gamma decrease osteoclast bone resorption activities, contributing to the enhanced trabecular bone volume and mineral density in these TG mice. These data suggest a novel role for this DLX-3 mutation in osteoclast differentiation and bone resorption.
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Registered trials
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.