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Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity with Drosophila developmental genes. Additionally we are shipping DLX3 Antibodies (57) and DLX3 Kits (2) and many more products for this protein.
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Results suggest that Dlx3 is a novel target of PKA, and that PKA mediates BMP signaling during osteoblast differentiation, at least in part, by phosphorylating Dlx3 and modulating its stability and function.
rs2278163 SNP of DLX3 might be associated with dental caries susceptibility in Japanese children. T and C alleles of rs2278163 SNP may potentially be involved in caries susceptibility and caries protection respectively.
In conclusion, results of our study suggest that the NOTCH (show NOTCH1 Proteins)-signaling pathway, which is activated during the osteogenic differentiation of DFCs.
DLX3 orchestrates the expression of multiple regulators of trophoblast differentiation and that expression of these regulatory genes is abnormal in fetal growth restriction.
DLX3 stimulates osteogenic differentiation via BMP2 (show BMP2 Proteins) dependent pathway.
Increased DLX3 expression in idiopathic fetal growth restricion (FGR (show FGR Proteins)) may contribute to trophoblast dysfunction observed in FGR (show FGR Proteins).
DLX3 acts upstream of syncytin (show ERVW-1 Proteins), 3beta-hydroxysteroid dehydrogenase, and the human gonadotropin beta-subunit (show POLG Proteins) to play a regulatory role in villous cytotrophoblast differentiation.
DLX3 homeodomain mutations cause tricho-dento-osseous syndrome with novel phenotypes
In cells expressing equal amounts of mutant and wild-type DLX3, deltaNp63alpha protein level was efficiently regulated, implying that heterozygosity at the DLX3 locus protects tricho-dento-osseous patients from severe p63 (show RPE65 Proteins)-associated skin defects.
SUMOylation of DLX3 by SUMO1 (show SUMO1 Proteins) promotes its transcriptional activity.
study demonstrates the co-expression of DLX3, PPARG (show PPARG Proteins) and SP1 (show SP1 Proteins) in trophoblast binucleated cell (BNC)nuclei; this suggests a possible role of these transcription factors through BNC specific genes at the time of pre-placental differentiation
DLX3 has a central role in controlling IFNT gene expression by associating with ETS2 on the IFNT promoter.
our data show that DLX3 promotes the expression of the EMP (show MAEA Proteins) genes Amelx (show AMELX Proteins), Enam (show ENAM Proteins), Klk4 (show KLK4 Proteins), and Odam (show ODAM Proteins) in amelogenesis.
The DLX3 regulates transcription factors crucial for bone formation and DLX3 attenuates bone mass accrual to support bone homeostasis by osteogenic gene pathway regulation.
We show that the deletion of Dlx3 in epidermis and isthums/infundibulum area leads to hair shaft differentiation but not hair growth.
we provide a novel insight that BMP-2 (show BMP2 Proteins)-induced Dlx3 expression is regulated by p38 (show CRK Proteins)/Smad5 (show SMAD5 Proteins) signaling pathway in osteoblasts.
used a conditional knockout approach to analyze the effects of neural crest deletion of Dlx3 on craniofacial bones development
regulation of Dlx3 by HR affects the IRS (show IARS Proteins) keratin expression, thus modulating the formation of IRS (show IARS Proteins) of hair follicle.
The transcription factor Dlx3 is essential in dentin formation by directly regulating a crucial matrix protein.
Dlx3 ablation in epidermis is linked to altered epidermal differentiation, barrier development, and IL-17 (show IL17A Proteins)-associated skin inflammation.
Mutant Dlx3 disrupts odontoblast polarization and dentin formation.
Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity with Drosophila developmental genes. Members of the Dlx gene family contain a homeobox that is related to that of Distal-less (Dll), a gene expressed in the head and limbs of the developing fruit fly. The Distal-less (Dlx) family of genes comprises at least 6 different members, DLX1-DLX6. Trichodentoosseous syndrome (TDO), an autosomal dominant condition, has been correlated with DLX3 gene mutation. This gene is located in a tail-to-tail configuration with another member of the gene family on the long arm of chromosome 17. Mutations in this gene have been associated with the autosomal dominant conditions trichodentoosseous syndrome and amelogenesis imperfecta with taurodontism.
distal-less homeobox 3
, distal-less homeo box 3
, DLX3 homeodomain containing protein
, homeobox protein DLX-3
, DII C