ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2010
DMP1 C-terminal mutant mice recapture the human ARHR tooth phenotype.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Cullin 4B-RING E3 ligase negatively regulates the immunosuppressive capacity of mesenchymal stem cells by suppressing iNOS.Cell death and differentiation · 2025Article
- CUL4B orchestrates mesenchymal stem cell commitment by epigenetically repressing KLF4 and C/EBPδ.Bone research · 2023Article
- Klf4 Promotes Dentinogenesis and Odontoblastic Differentiation via Modulation of TGF-β Signaling Pathway and Interaction With Histone Acetylation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- FGF23 and its role in X-linked hypophosphatemia-related morbidity.Orphanet journal of rare diseases · 2019Review
- Article
- Nucleus-targeted Dmp1 transgene fails to rescue dental defects in Dmp1 null mice.International journal of oral science · 2014Article
- Constitutive nuclear expression of dentin matrix protein 1 fails to rescue the Dmp1-null phenotype.The Journal of biological chemistry · 2014Article
- The rachitic tooth.Endocrine reviews · 2014Review
- Review
- The rescue of dentin matrix protein 1 (DMP1)-deficient tooth defects by the transgenic expression of dentin sialophosphoprotein (DSPP) indicates that DSPP is a downstream effector molecule of DMP1 in dentinogenesis.The Journal of biological chemistry · 2013Article
- Dentin matrix protein 1 and phosphate homeostasis are critical for postnatal pulp, dentin and enamel formation.International journal of oral science · 2012Article
- Dentin sialophosphoprotein and dentin matrix protein-1: Two highly phosphorylated proteins in mineralized tissues.Archives of oral biology · 2012Review
- Nuclear localization of DMP1 proteins suggests a role in intracellular signaling.Biochemical and biophysical research communications · 2012Article
- The chicken or the egg: PHEX, FGF23 and SIBLINGs unscrambled.Cell biochemistry and function · 2012Review
- Regulation of bone-renal mineral and energy metabolism: the PHEX, FGF23, DMP1, MEPE ASARM pathway.Critical reviews in eukaryotic gene expression · 2012Review
- ASARM peptides: PHEX-dependent and -independent regulation of serum phosphate.American journal of physiology. Renal physiology · 2011Article
- GEP, a local growth factor, is critical for odontogenesis and amelogenesis.International journal of biological sciences · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
DMP1 mutations in autosomal recessive hypophosphatemic rickets (ARHR) patients and mice lacking Dmp1 display an overlapping pathophysiology, such as hypophosphatemia. However, subtle differences exist between the mouse model and human ARHR patients. These differences could be due to a species specificity of human versus mouse, or it may be that the mutant DMP1 in humans maintains partial function of DMP1. In this study we report a deformed tooth phenotype in a human DMP1 deletion mutation case. Unexpectedly, the deletion of nucleotides 1484 to 1490 (c.1484_1490delCTATCAC, delMut, resulting in replacement of the last 18 residues with 33 random amino acids) showed a severe dentin and enamel defect similar to a dentinogenesis imperfecta (DI) III-like phenotype. To address the molecular mechanism behind this phenotype, we generated delMut transgenic mice with the endogenous Dmp1 gene removed. These mutant mice did not recapture the abnormal phenotype observed in the human patient but displayed a mild rachitic tooth phenotype in comparison with that in the Dmp1-null mice, suggesting that the DI III-like phenotype may be due to an as-yet-undetermined acquired gene modifier. The mechanism studies showed that the mutant fragment maintains partial function of DMP1 such as stimulating MAP kinase signaling in vitro. Last, the in vitro and in vivo data support a role of odontoblasts in the control of fibroblast growth factor 23 (FGF-23) regulation during early postnatal development, although this regulation on Pi homeostasis is likely limited.
Indexed as
Identifiers
What OpenQuestion holds
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.