Smad-binding defective mutant of transforming growth factor beta type I receptor enhances tumorigenesis but suppresses metastasis of breast cancer cell lines. Cancer Res 64, 4523-4530 (2004).Tian F,Byfield SD,Parks WT,et al.Smad-binding defective mutant of transforming growth factor beta type I ...
Stimulation of type I collagen transcription in human skin fibroblasts by TGF-beta: involvement of Smad 3. Smad-binding element in the plasminogen activator inhibitor-1 gene promoter was found within the TGF-β-response region of the proximal COL1A2 promoter. ... SJ Chen,W Yuan,Y Mori,......
Gel mobility shift assays showed protein phosphorylation-dependent binding activity in fibroblast nuclear extracts specific for this sequence; TGF-β treatment strongly stimulated the formation of this DNA-protein complex. Smad was identified as a component of the CAGACA-binding transcription complex in ...
The phosphorylation of Smad was repressed with the inhibitor, and the luciferase activity was cancelled using a mutant construct of Smad binding site of α2(I) collagen gene. However, the MAPK pathways, p38, ERK1/2 and JNK, were not affected with specific inhibitors or siRNA. The data ...
S. et al. SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling. Nat. Immunol. 18, 995–1003 (2017). Article CAS PubMed PubMed Central Google Scholar Myers, J. A. & Miller, J. S. Exploring the NK cell platform for cancer ...
The induction of SMYD3 in iTreg cells is mediated by a Smad-dependent mechanism As our data in Figure 1 indicated that TGFb was a primary inducer of SMYD3, we interrogated the SMYD3 promoter gene for Smad binding element (50-GTCTG-30).19 Three Smad binding elements were identified ...
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(IKKα), andIkbkb, along withTollip, Il33, Smad3, Il1rap, Traf6, andIl1rl1(Fig.2c). Interestingly, comparison of DEGs to a published dataset30in which astrocyte reactivity was induced indirectly in vivo by intraperitoneal administration of the endotoxin lipopolysaccharide (LPS) showed ...
We conclude that all the type I BMP receptors studied here (ALK2, ALK3, or ALK6) compete with ALK4 for binding to ACVR2A and that this competition modulates the signaling between the two distinct Smad pathways (Smad2/3 vs. Smad1/5/8). Discussion Activin and BMP receptors exhibit ...
Meanwhile, LA participated in the compound of collagen by TGF-β/Smad, Wnt/β-catenin, IL-6/STAT3 and promote EMT [40]. G protein-coupled receptor 81 (GPR81) as the receptor of LA could activate the Wnt pathway and regulate the proliferation and migration of cancer [68, 69]. Our ...