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TGFB increases the amount of SMAD2. 50 / 54
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"Furthermore, KLF10 overexpression enhanced the TGFbeta induced Smad2 phosphorylation and increased the transcription of Smad2, but not Smad3 or Smad4 [XREF_BIBR]."

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"Tgf-beta stimulation, which curbed sprouting, lead to high pSmad2 levels in all endothelial cells, an effect that was sensitive to the Alk5 inhibitor SB-431542."

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"Furthermore, this effect was specific to the BMP signaling pathway as there was no difference in the levels of phospho-Smad 2 following TGF-beta stimulation (XREF_FIG f)."

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"The result of Western blot showed that TGF-beta markedly enhanced p-Smad2 level, and also promoted FAST1 expression (XREF_FIG)."

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"While the expression level of Smad2 was not affected by miR-6315 treatment (p > 0.05, NC vs. miR-6315, Figure 7C), supplementation of TGF-β1 significantly induced Smad2 expression (p < 0.0005, NC vs. NC+TGF-β1)."
| PMC

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"Western blotting demonstrated that TGF-beta also enhanced the expression of p-Smad2 in both the active Yap1 group and the Yap1-ko group."

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"TGF-β induces the expression of SMAD2, which is a direct positive regulator of IL-17A expression (Th17 module, Fig. 2)."
| PMC

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"Recombinant TGF-β1 significantly enhanced the expression of TGF-β1, p-SMAD2, and vimentin and decreased the expression of E-cadherin, without altering the total SMAD2 levels (Fig. 2a, b)."

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"Additionally, TGF-beta treatment did not increase the levels of Smad2 and Smad4; however, TGF-beta treatment resulted in slightly increased levels of Smad3 protein."

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"The protein level of p-Smad2 was upregulated by TGF-β1 stimulation."

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"Combination of TGF-beta and MG132 during the treatment increased the levels of phospho-Smad2 over that of TGF-beta treatment alone, and showed a marked increase at 16 h."

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"The lanes 3–4 validate the function of the TGFβ1and TGFβ receptor inhibitor A8301; TGFβ1 upregulated the expression of p-Smad2, and A8301 inhibited the expression of p-Smad2, even in the E6 medium with TGFβ1."

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"TGFbeta treatment of C2C12 myoblasts stimulates C/EBPbeta expression which in turn stimulates the expression of Pax7 and Smad2 as well as autoregulating itself in both growth and differentiation conditions."

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"Pharmacological inhibition of TGFbeta signaling in Marfan SMCs with the TbetaR1 inhibitor LY364947 (LY) strongly reduced the high pSmad2 and pSmad3 levels, SMC differentiation marker expression, and mRNA levels for myocardin and SRF 53."

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"It has been demonstrated that although TGFbeta signaling is the major regulator of EMT and maintains the stem cell phenotype (Scheel et al., 2011), CD44s, but not the variant isoforms, plays an import[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, we observed that the TGF-β-induced expression of TGF-β1, Smad2, Smad3, COLI and COLIII was attenuated upon BMSC treatment in DFs, while the decrease in TGF-β3 expression was enhanced by BMSCs."

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"As a positive control, inclusion of exogenous TGF-beta in the cultures dramatically upregulated the levels of P-Smad2, which was positively correlated with the increase in Foxp3 + T cells."

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"38 In our study, TGFbeta induced an increase in p-Smad2 expression, which in turn promoted FoxC2 expression."

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"In agreement to this finding, TGF-beta could induce pSMAD2 and ZEB1 expression in GG14, whereas in GG16 cells, considerable expression of these proteins could already be detected."

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"Loss of Smad3 had essentially no effect on TGFbeta signaling through Smad2, as assessed by western blot analysis of Smad2 phosphorylation, whereas loss of Smad2 caused a slight reduction in the level of Smad3 phosphorylation by TGFbeta."

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"In U2OS 2G reporter cells (clone-17), a time course of TGFbeta induces similar levels of phospho-SMAD2, while GFP expression is also induced in a time dependent manner (XREF_FIG)."

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"TGFbeta signaling stimulates C/EBPbeta expression, which in turn increases Smad2 expression and Pax7 expression in myoblasts, inhibiting differentiation."

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"TGFbeta treatment of C2C12 myoblasts stimulates C/EBPbeta expression, which in turn can stimulate Pax7 and Smad2 expression, and inhibits myogenesis."

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"As shown in Fig. 6f, TGF-β1-induced expression of p-Smad2 was suppressed by treatment with NC siRNA/hypo-SF-MSC-CM."

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"In BMPR2 +/- PSCs, pSmad1/5/8 level was barely detectable upon BMP2 stimulation, while pSmad2 level was further enhanced by TGF-beta stimulation, compared to wild-type PSCs (P < 0.05)."

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"Phosphorylated level of SMAD2 or SMAD3 induced by TGFbeta was impaired when WTAP was silenced."

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"TGF-beta potently upregulated the expression levels of p-smad2 in both cell lines."

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"The expression of MADR2, but not of MADR1, was up-regulated by TGFbeta in vitro in a concentration- and time dependent manner."

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"In our study, we added TGFbeta to our coculture system, and the results showed that the expression of E-cadherin decreased slightly in TECs and that TGFbeta induced an increase in the level of p-Smad2, which in turn promoted the expression of FoxC2."

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"Interestingly, nonresponding cells displayed already high levels of pSMAD2 and ZEB1 that could not be suppressed by inhibition of TGF-beta signaling, suggesting the involvement of yet unknown mechanisms."

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"In the nonspecific siRNA transfection group, TGF-beta induced Smad3 protein expression, but not Smad2 protein expression."

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"ChIP analysis showed that in the absence of TGF-beta1, moderate levels of Smad2 and/or Smad3 and Smad4 were evident at the PPARgamma promoter, and activation of TGF-beta signaling enhanced the levels of Smad2 and/or Smad3 and Smad4 at the promoter region of the PPARgamma gene (XREF_FIG)."

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"TGF-beta is able to induce p-Smad2 levels and Smad7 (a well defined TGF-beta target gene) in neuroprogenitors to the same extent as in GBM neurospheres."

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"TGF-beta significantly increased the levels of p-SMAD2, p-SMAD3, p-AMPK, and p-ERK."

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"Of the selected kinase inhibitors, Lapatinib, AG1478 and LY294002 completely block TGFbeta induced Smad2 phosphorylation while Erlotinib, AG825, SP600125, SB203580, SB202190 and Staurosporine show only moderate reduction in measurable pSmad2 levels."

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"To investigate the potential antifibrotic effect of ME, Western blotting was used to assess the expression of α-SMA, Collagen I, Collagen III, pSMAD2, pSMAD3, TIMP1, TIMP3 and MMP3 induced by TGF-β1 in CCD-18Co cells treated with or without different concentrations of ME."

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"Our results showed that TGF-beta could induce the p-SMAD2, p-SMAD3, EGFR and IGFBP-3 expression."

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"As shown in Figure 4 A, the P-Smad2 level induced by TGFbeta was diminished in the presence of human PPM1A (lane 2) but was restored by coexpression of shPPM1A494, correlating with the depleted level [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Despite robust upregulation of C/EBPbeta expression in TGFbeta treated C2C12 myoblasts, and a role for C/EBPbeta in the maintenance of Smad2 mRNA expression under growth conditions in primary myoblasts, we failed to observe a consistent upregulation of Smad2 or Cebpb expression by TGFbeta in the primary myoblasts, while Pax7 was upregulated."

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"By contrast, TGF-beta induced accumulation of cells at G0/G1, and upregulated expression of p-JNK, p-c-Jun and p-smad2."

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"Moreover, increased expression of pSmad2, ZEB1, vimentin, and Slug induced by TGF-beta was reversed upon treatment with LY2157299."

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"Importantly, addition of recombinant TGF-beta ligands to the Shh cre : Hdac3 f/f mutant epithelial cell culture increased p-Smad2 expression and partially restored the ability of AT1 cells to spread (XREF_SUPPLEMENTARY, and XREF_FIG)."

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"To check the effectiveness of FST288 on cultured ovaries, we measured the phosphorylation level of smad2 which could be activated by TGF-beta superfamily members in the ovaries."

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"Indeed, TGFbeta increased phosphorylation levels of Smad2 and Smad3 in VSMCs."

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"Finally, recombinant TGF-beta significantly increased the phosphorylation levels of SMAD 2 and SMAD 3 in DFAT cells."

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"We found that suppression of TGF-beta signaling by the inhibitor reduced Smad2 phosphorylation level and down-regulated Vimentin expression, without affecting the morphologic and molecular features of c-kit-expressing ACC-M cells undergoing EMT."

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"Inhibition of TGF-beta receptor signaling by a TGF-beta RI kinase inhibitor (ALK5 inhibitor) abolished TGF-beta-induced phosphorylation of Smad2, Smad3 and PTHrP protein expression (XREF_FIG), although ALK5 inhibitor alone induced PTHrP expression."

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"In contrast, the inhibition of TGF-β1 receptors decreased the expression of Smad2, Smad3, p38, and Erk1/2 and the formation of the Smad2/3/4 complex."

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"In addition, PYP1-5 activated the TGF-beta and Smad signaling pathway, which increased TGF-beta1, p-Smad2 and p-Smad3 expression, while inhibiting Smad7, an inhibitor of the TGF-beta and Smad pathway."

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"We found that TGF-β1 treatment increased phospho-Smad2 and p35 protein levels, and this increase was blocked in cells co-treated with SB431542 (Figure 4B)."