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Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity with Drosophila developmental genes. De plus, nous expédions DLX3 Protéines (6) et DLX3 Kits (4) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 57 products:
Human Polyclonal DLX3 Primary Antibody pour ELISA, WB - ABIN560618
Pálmer, Anjos-Afonso, Carmeliet, Takeda, Watt: The vitamin D receptor is a Wnt effector that controls hair follicle differentiation and specifies tumor type in adult epidermis. dans PLoS ONE 2008
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Human Monoclonal DLX3 Primary Antibody pour ELISA, WB - ABIN515013
Viale-Bouroncle, Gosau, Morsczeck: NOTCH1 signaling regulates the BMP2/DLX-3 directed osteogenic differentiation of dental follicle cells. dans Biochemical and biophysical research communications 2014
Cow (Bovine) Polyclonal DLX3 Primary Antibody pour WB - ABIN2780658
Schlögl, Keinrath, Zimmermann, Scherer, Leeb, Pfurtscheller: A fully automated correction method of EOG artifacts in EEG recordings. dans Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology 2006
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DLX3 regulates bone marrow mesenchymal stem cell proliferation through H19 (Montrer NCKAP1 Anticorps)/miR (Montrer MLXIP Anticorps)-675 axis.
Data establish the DLX3-p53 (Montrer TP53 Anticorps) interplay as a major regulatory axis in epidermal differentiation and suggest that DLX3 is a modulator of skin carcinogenesis.
Identify a novel cis (Montrer CISH Anticorps)-acting sequence (-369 to -320) at the placental growth factor (Montrer PGF Anticorps) promoter, which was critical for mediating the basal and DLX3/GCM1 (Montrer GCM1 Anticorps)-dependent PGF (Montrer PGF Anticorps) promoter activities.
We showed that the supplementation of the osteogenic differentiation medium with PTHrP (Montrer PTHLH Anticorps) inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3, but the depletion of PTHrP (Montrer PTHLH Anticorps) did not support the differentiation of DFCs.We showed that SUFU (Suppressor Of Fused Homolog (Montrer SUFUH Anticorps)) 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 (Montrer ESR1 Anticorps) 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 (Montrer NOTCH1 Anticorps)-signaling pathway, which is activated during the osteogenic differentiation of DFCs.
study demonstrates the co-expression of DLX3, PPARG (Montrer PPARG Anticorps) and SP1 (Montrer SP1 Anticorps) 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 (Montrer MAEA Anticorps) genes Amelx (Montrer AMELX Anticorps), Enam (Montrer ENAM Anticorps), Klk4 (Montrer KLK4 Anticorps), and Odam (Montrer ODAM Anticorps) 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 (Montrer BMP2 Anticorps)-induced Dlx3 expression is regulated by p38 (Montrer CRK Anticorps)/Smad5 (Montrer SMAD5 Anticorps) 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 (Montrer IARS Anticorps) keratin expression, thus modulating the formation of IRS (Montrer IARS Anticorps) 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 (Montrer IL17A Anticorps)-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