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Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity with Drosophila developmental genes. Zusätzlich bieten wir Ihnen DLX3 Proteine (7) und DLX3 Kits (3) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal DLX3 Primary Antibody für 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. in PLoS ONE 2008
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Human Monoclonal DLX3 Primary Antibody für 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 für 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
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Our research of DLX3 mutation protecting aging-related bone loss opens the possibility of its therapeutic potential in bone regeneration and bone loss disease.
DLX3 expression specifically modulates regulatory networks such as Wnt (zeige WNT2 Antikörper) signaling, phosphatase activity and cell adhesion.
Novel de novo mutation of DLX3 significantly decreases the proliferation rate and inhibits the odontogenic differentiation and mineralization of hDPCs, suggesting that this novel mutation of DLX3 can influence the dentinogenesis in TDO syndrome.
DLX3 regulates bone marrow mesenchymal stem cell proliferation through H19 (zeige NCKAP1 Antikörper)/miR (zeige MLXIP Antikörper)-675 axis.
Data establish the DLX3-p53 (zeige TP53 Antikörper) interplay as a major regulatory axis in epidermal differentiation and suggest that DLX3 is a modulator of skin carcinogenesis.
Identify a novel cis (zeige CISH Antikörper)-acting sequence (-369 to -320) at the placental growth factor (zeige PGF Antikörper) promoter, which was critical for mediating the basal and DLX3/GCM1 (zeige GCM1 Antikörper)-dependent PGF (zeige PGF Antikörper) promoter activities.
We showed that the supplementation of the osteogenic differentiation medium with PTHrP inhibited the alkaline phosphatase activity and the expression of the transcription factor DLX3, but the depletion of PTHrP did not support the differentiation of DFCs.We showed that SUFU (Suppressor Of Fused Homolog (zeige SUFUH Antikörper)) 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 (zeige ESR1 Antikörper) regulates the osteoblast differentiation through modulation of Dlx3 expression and/or interaction with Dlx3.
study demonstrates the co-expression of DLX3, PPARG (zeige PPARG Antikörper) and SP1 (zeige SP1 Antikörper) 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.
DLX3 is indispensable for the regulation of ion transporters and carbonic anhydrases during the maturation stage of amelogenesis, exerting a crucial regulatory function on pH oscillations during enamel mineralization.
our data show that DLX3 promotes the expression of the EMP (zeige MAEA Antikörper) genes Amelx (zeige AMELX Antikörper), Enam (zeige ENAM Antikörper), Klk4 (zeige KLK4 Antikörper), and Odam (zeige ODAM Antikörper) in amelogenesis.
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.
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 (zeige BMP2 Antikörper)-induced Dlx3 expression is regulated by p38 (zeige CRK Antikörper)/Smad5 (zeige SMAD5 Antikörper) 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 (zeige IARS Antikörper) keratin expression, thus modulating the formation of IRS (zeige IARS Antikörper) of hair follicle.
The transcription factor Dlx3 is essential in dentin formation by directly regulating a crucial matrix protein.
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