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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 Proteins (6) and DLX3 Kits (2) and many more products for this protein.
Showing 10 out of 56 products:
Cow (Bovine) Polyclonal DLX3 Primary Antibody for WB - ABIN2780658
Schlögl, Keinrath, Zimmermann, Scherer, Leeb, Pfurtscheller: A fully automated correction method of EOG artifacts in EEG recordings. in Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology 2006
Show all 2 references for ABIN2780658
Cow (Bovine) Polyclonal DLX3 Primary Antibody for WB - ABIN2777374
Lee, Lee, Lee, Ahn, Kim, Lee, Kim: DLX3 mutation in a new family and its phenotypic variations. in Journal of dental research 2008
Human Monoclonal DLX3 Primary Antibody for ELISA, WB - ABIN515013
Viale-Bouroncle, Gosau, Morsczeck: NOTCH1 signaling regulates the BMP2/DLX-3 directed osteogenic differentiation of dental follicle cells. in Biochemical and biophysical research communications 2014
Cow (Bovine) Polyclonal DLX3 Primary Antibody for IHC, WB - ABIN2779508
Morsczeck: Gene expression of runx2, Osterix, c-fos, DLX-3, DLX-5, and MSX-2 in dental follicle cells during osteogenic differentiation in vitro. in Calcified tissue international 2006
We showed that the supplementation of the osteogenic differentiation medium with PTHrP (show PTHLH Antibodies) inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3, but the depletion of PTHrP (show PTHLH Antibodies) did not support the differentiation of DFCs.We showed that SUFU (Suppressor Of Fused Homolog (show SUFUH Antibodies)) was not regulated during the osteogenic differentiation in DFCs
we identified a recurrent 2-bp deletion in the DLX3 gene in a new family and described their mild clinical phenotype related to the DLX3 mutation.
genetic analysis revealed a novel de novo missense mutation c.533A>G (p.Q178R) in the conserved homeodomain of the DLX3 gene. This DLX3 mutation is the sixth causative mutation for TDO to be identified so far.
ER-alpha (show ESR1 Antibodies) regulates the osteoblast differentiation through modulation of Dlx3 expression and/or interaction with Dlx3.
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 Antibodies)-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 Antibodies) dependent pathway.
Increased DLX3 expression in idiopathic fetal growth restricion (FGR (show FGR Antibodies)) may contribute to trophoblast dysfunction observed in FGR (show FGR Antibodies).
study demonstrates the co-expression of DLX3, PPARG (show PPARG Antibodies) and SP1 (show SP1 Antibodies) 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 Antibodies) genes Amelx (show AMELX Antibodies), Enam (show ENAM Antibodies), Klk4 (show KLK4 Antibodies), and Odam (show ODAM Antibodies) 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 Antibodies)-induced Dlx3 expression is regulated by p38 (show CRK Antibodies)/Smad5 (show SMAD5 Antibodies) 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 Antibodies) keratin expression, thus modulating the formation of IRS (show IARS Antibodies) 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 Antibodies)-associated skin inflammation.
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