DLX3 antibody - N-terminal region (ARP31605_P050)
- Known as:
- DLX3 (anti-) - N-terminal region (ARP31605_P050)
- Catalog number:
- arp31605_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DLX3 antibody - N-terminal region (ARP31605_P050)
Related genes to: DLX3 antibody - N-terminal region (ARP31605_P050)
- Gene:
- DLX3 NIH gene
- Name:
- distal-less homeobox 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-16
- Date modifiied:
- 2015-08-25
Related products to: DLX3 antibody - N-terminal region (ARP31605_P050)
Related articles to: DLX3 antibody - N-terminal region (ARP31605_P050)
- DLX3 is a homeobox transcription factor essential for multiple organogenesis processes. Mutations in DLX3 cause trichodentoosseous syndrome (TDO), characterized by curly hair, sclerotic bone, enamel, and dentin defects as well as taurodontism. Phenotypic variability in TDO has been well documented, but its pathogenesis remains poorly understood. Here, we characterized three TDO families with distinct clinical features and identified a known DLX3 deletion (c.561_562del) and the first pathogenic splice-site variant (c.516+1_516+2insA). The proband with the splice-site mutation displayed a mesenchymal-dominant phenotype with severe dentin hypoplasia, enlarged pulp chambers, and hypertaurodontism but nearly normal enamel, whereas the mother and sister showed epithelial-dominant anomalies, including enamel hypoplasia and kinky hair. Minigene analysis demonstrated that c.516+1_516+2insA generated two aberrant transcripts encoding p.Val173Aspfs*28 and p.Arg120_Val173del. These mutant proteins localized mainly in the cytoplasm and showed markedly reduced transactivation activity. In cultured human dental pulp cells, DLX3 overexpression upregulated the odontoblastic markers DSPP, MMP20, and WNT10A. Chromatin immunoprecipitation and reporter assays further revealed that DLX3 directly activates WNT10A via a conserved enhancer (chr2:218,878,973_218,879,302) and three upstream binding sites. These findings expand the TDO mutational spectrum and suggest that differential mutant DLX3 expression may contribute to phenotypic variability, whereas disrupted regulation of WNT10A underlies dentin defects and taurodontism. - Source: PubMed
Wang Yin-LinLin Hua-ChiehChen Jung-TsuChang Hsiao-HuaHsieh Ting-FengHung Hsin-YaWang Shih-Kai - Enamel, the hardest mineralized material in the human body, protects the underlying living tissues, the dentin and pulp of the tooth. However, over 90% of adults have lost or damaged enamel and cannot regenerate the protective structure due to lack of enamel-producing cells, ameloblasts. iPSC-derived secretory Ameloblasts (isAM) have promise in future regenerative dentistry. Today, it is not known why iAM maturation requires intimate contact with the dentin-producing cell type, odontoblast. Here, we reveal that one of the critical signaling ligands emanating from odontoblasts for ameloblast maturation is Delta, the ligand for Notch receptor. We showed that our designed, soluble Notch agonist can induce iAM organoid maturation in an unprecedented manner, without interactions with odontoblast layer. Notably, soluble Notch agonist induces the iAM maturation to a novel, WDR72-positive mature secretory AM stage (ismAM) in our ameloblast organoid model. When transplanted under the kidney capsule of NOD-SCID mice, these ismAM organoids generated enamel-like calcified material, as confirmed by microCT analysis, marking the first demonstration that Notch-activated iAM organoids can form such tissue in vivo. This novel maturation procedure enabled us to analyze the specific requirements of DLX3 function in ameloblasts, independent of its known function in odontoblasts. We now show that DLX3, a gene associated with Amelogenesis Imperfecta, is required on a cell-autonomous manner in human ameloblasts for the expression of Enamelin, MMP20, and WDR72, a role not previously demonstrated in mouse models. - Source: PubMed
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