IndraLab

Statements


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"These findings showed that a single missense mutation in Smad3 could specifically block TGF-beta signals by preventing activation of both Smad2 and Smad3."

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"Knockout of Smad3 blocks TGF-beta-induced EMT in primary tubular epithelial cells, and the reduction of Smad2 and Smad3 function is associated with the decreased metastatic potential of breast cancer cell lines in a xenograft model [XREF_BIBR]."

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"Furthermore, the knockdown of SMAD4 or SMAD2 but not SMAD3 abolished the inhibitory effects of all three activin isoforms on StAR expression."

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"Additionally, we identify that PRMT1 knockdown results in down-regulation of TGF-beta1, p-Smad2 and p-Smad3, while PRMT1 overexpression activates TGF-beta1, p-Smad2 and p-Smad3."

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"The location of SMAD2 and SMAD3 in the cytoplasmic and nuclear fractions of RIE-1-TrkB cells block nuclear localization of SMAD2 and SMAD3 in response to TGF-beta."

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"Knockout of Smad3 blocks TGF-beta-induced EMT in primary tubular epithelial cells, and the reduction of Smad2 and Smad3 functions are associated with the decreased metastatic potential of breast cancer cell lines in a xenograft model [XREF_BIBR]."

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"These results support that Smad2 but not Smad3 functions as a tumor suppressor in NRP-152 cells, although loss of Smad3 enhanced tumor growth and incidence in the Smad2 deficient cells."

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"Our data show that during PCMO generation pluripotency marker expression is controlled positively by activin and Smad2 and negatively by TGF-beta and Smad3 signaling, while relief from growth inhibition is primarily the result of reduced TGF-beta and Smad3, and to a lesser extent, activin and Smad2 signaling."

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"Knockdown of Smad2, but not Smad3, led to disruption of pIgR-Smad interactions, suggesting that pIgR plays a direct role in recruiting Smad2 (XREF_FIG)."

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"Depletion of SMAD2, but not SMAD3, significantly abolished the inhibitory effects of TGFbeta1 on the growth of GBM cells, possibly through pSMAD2 mediated increases in cell-cycle inhibitor, p27."

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"In this study, we investigated that although Smad2 and Smad3 are structurally similar with 89% amino acid sequence similarity in bovine, Smad3 significantly decreased Smad2 mRNA and protein expression during bovine myoblast differentiation, which is not by binding on its promoter."

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"Loss of Smad2 and Smad4, but not Smad3 is common in human cancers."

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"As shown in Fig. 5, Smad2 and Smad3 siRNA specifically down-regulated Smad2 and Smad3, respectively, in both SKOV3 and OVCAR4 cells."

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"Smurf2and Skp1-Cul1F-box protein (SCF), the Smad2 and Smad3 E3 ubiquitin ligase, respectively, mediates the degradation of Smad2 and Smad3."

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"In the mouse goosecoid promoter, Smad2 was found to activate the gene in cooperation with FAST2, whereas Smad3 was unable to activate the element and blocked Smad2 dependent activation [39]."

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"The mutant, Smad3 (DE), blocked the activation of wild-type Smad2 and Smad3."

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"The reduction in occupancy was accompanied by a significant decrease in Smad2 mRNA expression in RA treated cells in both growth medium and under differentiation conditions, indicating that Smad2 is a C/EBPbeta target gene in this system, and raising the possibility that RA upregulated Smad3 could prevent Smad2 upregulation and thereby promote myogenesis."

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"To examine whether Smad3 could function to negatively regulate the Smad2 and Smad4 mediated response, cells were transfected with FAST2, Smad2, and Smad4 along with increasing concentrations of Smad3."

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"Activation of Ca2 +/calmodulin-dependent protein kinase II (CamKII) also results in Smad2, Smad3 and Smad4 phosphorylation inhibiting TGF-beta-induced nuclear import and transcriptional activity of Smad2, and affecting Smad heteromerization [XREF_BIBR]."

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"These results demonstrate that inhibiting TGF-beta signaling with SB-431542 blocks phosphorylation of Smad2 and Smad3 and prevents nuclear translocation of p-Smad2 and p-Smad3, which ultimately interrupts bladder smooth muscle formation."