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SP7 encodes a member of the Sp subfamily of Sp/XKLF transcription factors. Additionally we are shipping SP7 Antibodies (37) and SP7 Kits (26) and many more products for this protein.
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Osterix decreased the chemosensitivity of breast cancer cells by upregulating the expression of GALNT14 (show GALNT14 Proteins), which eventually suppressed the apoptosis of breast cancer cells.
TP(thymidine phosphorylase (show TYMP Proteins) ) curbed the expression of three proteins-IRF8 (show IRF8 Proteins), RUNX2 (show RUNX2 Proteins), and osterix. This downregulation was epigenetically driven: High levels of 2DDR, a product of TP secreted by myeloma cells, activated PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) signaling and increased the methyltransferase DNMT3A's expression
dissection of these interconnected epigenetic mechanisms that govern Sp7 gene activation reveals a hierarchical process where regulatory components mediating DNA demethylation play a leading role
SP7 gene promoter is robustly enriched in epigenetic repressive marks that may explain its poor transcriptional response to osteoblast differentiating media in umbilical cord derived mesenchymal stem cells.
Eight and five of the nine samples were negative for cell adhesion molecule 1 (show CADM1 Proteins) and Osterix respectively. The other markers showed no statistical significance(CD151 (show CD151 Proteins),ALP (show ALP Proteins)). osteoblastic differentiation can occur in carcinoma cells and that cell adhesion molecule 1 (show CADM1 Proteins) could be a useful marker for identifying this phenomenon in carcinoma tissues
The results suggest that Osterix plays an important role in increasing BMP- 4 (show BMP4 Proteins)-induced Cx43 (show GJA1 Proteins) activity.
The expression of specific targets Smad1 (show GARS Proteins) and Osterix was significantly increased in the presence of Pi and restored by coincubation with Mg(2 (show MUC7 Proteins)+). As miR (show MLXIP Proteins)-30b, miR (show MLXIP Proteins)-133a, and miR (show MLXIP Proteins)-143 are negatively regulated by Pi and restored by Mg(2 (show MUC7 Proteins)+) with a congruent modulation of their known targets Runx2 (show RUNX2 Proteins), Smad1 (show GARS Proteins), and Osterix, our results provide a potential mechanistic explanation of the observed upregulation of these master switches of o
Preameloblast-Derived Factors Mediate Osteoblast Differentiation of Human Bone Marrow Mesenchymal Stem Cells by Runx2 (show RUNX2 Proteins)-Osterix-BSP (show KLK6 Proteins) Signaling.
Osx (show MID1 Proteins) might function as a potential regulator for the proliferation and odontoblastic differentiation of hDPCs.
Data suggest that beta-catenin (beta-cat) signaling upregulates the expression of osterix (OSX) in pre-osteoblastic and bone marrow stromal cells.
Sp7 plays a critical role in limiting the level of signaling and the rate of bone growth
FGF and Wnt (show WNT2 Proteins)/beta-Catenin (show CTNNB1 Proteins) pathways act in part by directing transcription of osx to promote osteoblast differentiation at sites of bone formation.
Data show the endogenous sp7 gene expression in the otic placode and vesicle, and in forming skeletal structures in Tg(sp7:EGFP)b1212 line.
These results suggest proliferation and maturation of immature osteoblasts requires Tgfbr2 (show TGFBR2 Proteins) signaling and that decreased bone volume in Osx-Cre;Tgfbr2 (show TGFBR2 Proteins)(fl/fl (show FLT3LG Proteins)) mice is likely due to fewer mature osteoblasts.
DNA damage and senescence in osteoprogenitors expressing Osx may cause their decrease with age.
The data support a model in which Dlx recruitment of Sp7 to osteoblast enhancers underlies Sp7-directed osteoblast specification.
Mmp13 (show MMP13 Proteins) is selectively regulated of by 1,25-Dihydroxyvitamin D3, PTH (show PTH Proteins), and Osterix through distal enhancers.
These results indicated that olfactory bulb development was not significantly impaired in the absence of Osx.
Wnt3a (show WNT3A Proteins) induces Osx expression via p38 MAPK (show MAPK14 Proteins) signaling in dental follicle cells. Wnt3a (show WNT3A Proteins)-induced Osx expression was inhibited in the presence of p38 mitogen-activated protein kinase (show MAPK14 Proteins) (MAPK (show MAPK1 Proteins)) inhibitors (SB203580 and SB202190) at gene and protein levels, as assessed by real-time PCR and immunocytohistochemistry, respectively.
Transfection assay demonstrated that Osx was able to activate Bsp (show KLK6 Proteins) promoter reporter in a dose-dependent manner. To define minimal region of Bsp (show KLK6 Proteins) promoter activated by Osx, a series of deletion mutants of Bsp (show KLK6 Proteins) promoter were generated, and the minimal region was narrowed down to the proximal 100 bp. Point-mutagenesis studies showed that one GC-rich (show RELB Proteins) site was required for Bsp (show KLK6 Proteins) promoter activation by Osx.
OSX served a key role in the development and progression of ALD-induced VSMC calcification. This observation may aid in the explanation of the role of OSX in the pathogenesis of vascular calcification
results suggest that expression of Sp7 during the early stage of Satb2 (show SATB2 Proteins)-induced osteogenic differentiation of BMSCs is regulated by miR (show MLXIP Proteins)-27a.
Fibrillin-2 (show FBN2 Proteins) and periostin (show POSTN Proteins) are target genes in Osterix-mediated osteoblast differentiation.
This gene encodes a member of the Sp subfamily of Sp/XKLF transcription factors. Sp family proteins are sequence-specific DNA-binding proteins characterized by an amino-terminal trans-activation domain and three carboxy-terminal zinc finger motifs. This protein is a bone specific transcription factor and is required for osteoblast differentiation and bone formation.
transcription factor Sp7
, zinc finger protein osterix
, transcription factor osterix
, Sp7 transcription factor
, transcription factor Sp7-like
, trans-acting transcription factor 7
, Sp7 transcription factor 7