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TGFB1 increases the amount of SMAD3. 60 / 68
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"Meanwhile, the immunofluorescence staining result also showed that TGF-beta1 increased the expression of pSmad3; on the contrary, curcumin decreased the expression of pSmad3 and inhibited nuclear translocation of pSmad3 (XREF_FIG)."

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"Furthermore, the levels of p-Smad3 and collagen I induced by TGFbeta1 were slightly increased after the addition of the recombinant human SDC-1 protein to Beas-2B and HLF-1 cells."

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"TGF-beta1 also induced Smad3, miR-192 and p-Smad3 expression, but suppressed E-cadherin expression."

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"As shown in XREF_FIG, western blotting results demonstrated that TGF-beta1 significantly increased the levels of Smad-2 phosphorylation and moderately enhanced Smad-3 phosphorylation."

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"The results showed that TGF-beta1 induced the expression of CTGF, COL I, p-Smad3 and Smad7 in a time dependent manner."

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"However, the selective inhibitor of the TGF-beta1 and Smad signaling pathway, SB431542, significantly decreased the protein expression of TGF-beta1, p-Smad2 and Smad2, p-Smad3 and Smad3 and Smad7 in NFs."

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"In the same series of experiments, we observed that endogenous TGFbeta1, like RAC1B [XREF_BIBR], promoted the expression of SMAD3 (XREF_FIG)."

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"Our findings revealed that the transfection of TGF-beta1 promoted the expressions of TGF-beta1 and Smad3, playing a protective role in ischemic stroke, and this protective role was illustrated by reduced infarct size."

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"The administration of TGF-beta1 increased the migration and invasion of EVI5-knockout NSCLC cells, and increased the levels of p-Smad3 and its downstream signaling molecules, indicating a therapeutic role for EVI5 in inhibition of cancer metastasis."

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"SB431542 inhibited TGFbeta1 induced SMAD3 phosphorylation and abrogated the small basal expression of pSMAD3 seen in control cultures without exogenous TGFbeta, indicating autocrine activity (XREF_FIG), as the growth medium supplements contained minimal TGFbeta activity and did not account for the baseline activity (XREF_SUPPLEMENTARY)."

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"Exogenous TGF-beta1 induced temporally dependent alterations in Smad2 and Smad3 gene expression."

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"In addition, knockdown of eIF3a suppressed TGF-beta-induced HSC proliferation and the expression of alpha-smooth muscle actin (alpha-SMA) and collagen I. Furthermore, knockdown of eIF3a inhibited the expression of p-Smad3 induced by TGF-beta1 in HSCs."

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"As expected, TGF-beta1 addition to the culture of TKPT increased expression levels of p-Smad3."

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"A recent study reports that naringenin significantly inhibits the transcription of SMAD3 induced by TGF-beta1 and reduces the probability of TGF-beta1 binding to its receptor TbetaRII, thereby inhibiting receptor dimerization and downstream signaling transduction, inhibiting cell migration and invasion."

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"Finally, to determine if TGFbeta signaling pathway was activated in cervical tissue we evaluated the expression of Smad2 and Smad3 which are known to be activated by TGFbeta1."

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"Furthermore, TGF-beta1 induces Smad3 expression to regulate microRNAs and Smad ubiquitination regulatory factor (Smurf) to exert its pro fibrotic effect."

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"We used recombinant human TGF-beta1 (2ng/ml) to stimulate HDFs for 24h, which showed TGF-beta1 significantly induced the Smad3 mRNA expression and downregulated the IL-17RA and IL-17RC expression on HDFs (P < 0.01; Figure XREF_FIG B)."

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"Then, transfecting A549 cells with HBLV-h-STAT3 revealed that overexpression of STAT3 can significantly increase the expression of p-SMAD3 induced by TGF-beta1 (XREF_FIG)."

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"The addition of TGF-beta2 (2 ng/mL), but not TGF-beta1, restored the levels of p-ERK1/2, p-Smad3, and alpha-SMA (XREF_FIG)."

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"Treatment of TGF-beta1 further increased the expressions of TGF-beta1 and Smad3, whereas the TGF-beta1 inhibitors group exhibited lower expressions of TGF-beta1 and Smad3 than those of the model and TGF-beta1 group (all P < 0.05)."

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"Moreover, TGF-beta1 supplement significantly restored Erk1/2 and SMAD3 phosphorylation levels individually or simultaneously which is inhibited by LAE supplement in three subtypes of breast cancer cells."

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"Confocal immunofluoresence assay with anti-pSmad3 antibody (used to detect levels of Smad3 when phosphorylated at Ser423/425) showed that TGF-beta1 treatment increased pSmad3 levels in VSMCs, especially in the nucleus; and pretreatment with 3AB or PJ34 prevented the TGF-beta1-induced increase (XREF_FIG)."

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"TGF-beta1 increased the invasive ability of JEG-3 cells and the expression levels of Smad2 and Smad3; hence, TGF-beta1 promotes the invasion of JEG-3 probably by activating Smad2 and Smad3."

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"Protein expressions of p-Smad3, PI3K, p-Akt and p-GSK-3beta were significantly up-regulated by stimulation of TGF-beta1."

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"TGFbeta1 promoted the expression of c-JUN, SMAD3 and p-SMAD3 and suppressed miR200a expression and SB431542 reversed these effects (XREF_FIG)."

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"The protein expression levels of p-Smad2 and p-Smad3, which are enhanced by TGF-beta1, were markedly decreased in Rg3 treated KFs (XREF_FIG)."

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"Similarly, our results showed that TGF-beta1 could increase the protein expression of p-Smad3 and TWIST1/2 in both HEC-1A and Ishikawa cells at 8 h. ISL is a flavonoid that showed anti-tumor effects in variety of cancer cells."
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"We found that low concentrations of TGF-beta1 inhibited the expression of P-AKT and promoted the expression of P-Smad3, while high TGF-beta1 concentrations had the opposite effect (XREF_FIG - XREF_FIG)."

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"The strong elevation in Cox-2 expression following TNFalpha+ TGFbeta1 stimulation was almost totally abrogated by joint siRNA induced downregulation of p65 and Smad3 expression."

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"In cultured neonatal myocardial cells, different level TGF-beta1 could significantly increase the total protein, and TGF-beta1 (3 ng/ml) could increase the expression of mRNA and protein of Smad3 and continued for 8 h of cultured cardiomyocytes."

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"TGF-beta1 increased the expression of NFYA, TGFbetaR1, TGFbetaR2, p-Smad2, p-Smad3, p-Smad3L, and p-Akt (Ser473), and knocking down NFYA decreased the expression of these genes, except for TGFbetaR2."

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"We firstly examined the expression of Smad2 and Smad3 induced by TGF-beta 1 in normal NIH/3T3 cells."

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"Because TGF-beta1 can induce p-Smad3 expression, 17 we treated lung adenocarcinoma cells with different concentrations of TGF-beta1 (0-20ng/ml)."

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"Western blot analysis revealed a high level of p-Smad2 and p-Smad3 in response to a 1-hour treatment with TGF-beta1."

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"Levels of p-SMAD3 were increased less than two-fold by TGFbeta1 at 48 hours and not at all at 96 hours."

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"Western-blot assay also showed that TGF-beta1 treatment increased pSmad3 levels in whole and nuclear extracts; and knockdown of PARP1 by siRNA or inhibition of PARP activity by 3AB or PJ34 prevented TGF-beta1-induced pSmad3 increase in both whole and nuclear extracts (XREF_FIG)."

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"The levels of phospho-SMAD3, which were increased by TGF-beta1 treatment, were decreased by eupatolide treatment in a time dependent manner (XREF_FIG)."

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"TGF-beta1 significantly induced the expression of Smad3 mRNA and downregulated the IL-17RA and IL-17RC expression on HDFs."

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"We then co-treated CFs with Ex-527, TGF-β, and RES and found that Ex-527 offset the effect of RES on TGF-β1–induced increased Ac-Smad3 protein expression in CFs ( xref )."

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"Consistent with the reduction in phosphorylated Smad3 by ASTX, the nuclear translocation of Smad3 was also reduced by ASTX, whereas TGFbeta1 treatment increased nuclear Smad3 levels."

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"TGF-beta1 can upregulate the expression of Smad2 and Smad3 during tissue fibrosis, a process that is negatively regulated by Smad7 as part of a negative feedback loop."

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"Consistent with XREF_FIG, Losartan blocked the TGFbeta1 mediated increase in p-ERK but levels of p-SMAD3 were not modulated by TGFbeta1 or by the inhibitors (XREF_FIG)."

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"Western Blot (WB) analysis suggested that TGF-beta1 treatment could effectively increase the expression of alpha-SMA, COL1, Smad3, and p-Smad3, which could be inhibited by SIS3 treatment."

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"The results revealed that TGF-beta1 promotes Smad3 transcription."

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"In the present study, TGF-beta1 treatment was shown to increase the phosphorylation levels of Smad2 and Smad3, confirmed by the enhancement of the transcription and expression of collagen mRNA shown in XREF_FIG, XREF_FIG, XREF_FIG."

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"Regulation of TbetaR1, SMAD4, SMAD3, SMAD7 and TIMP-1 mRNA expression by TGF-beta1 in HTR-8 and SVneo cells."

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"Following transfection of A549 cells with miR-320a-3p mimic, the expression of p-SMAD3 induced by TGF-beta1 was significantly reduced, while total SMAD3 was unaffected (XREF_FIG)."

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"TGF-beta1 increased the expression of TGFbetaR1, p-p70S6K, p300, p-Smad3, p-Smad3L, PDGFRbeta, p-ERK, and alphaSMA in Lx-2 cells, and this activation was repressed by the addition of BCAA."

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"NOF-CAF cells ' expression of p-SMAD2 and p-SMAD3 in response to TGF-beta1 demonstrated intact TGF-beta signaling."

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"In choriocarcinoma cells, the expression of Smad3 could be promoted by TGF-beta1, and suppressed by p38 MAPK inhibitor [XREF_BIBR]."

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"TGF-beta1 increased the expression of type I collagen and Smad3 protein in d4 primary HSCs, while SA-B inhibited their expression."

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"TGF-beta1 promotes the expression of Smad3 and inhibits the expression of Smad7 during the activation of PSCs."

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"Correlation of Promoter Binding by SMAD3 and Altered Gene Expression by TGFbeta1."

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"The underlying mechanism might be the down-regulated expression of AT1R mRNA and Smad-3, increased production of Smad-7, and blocking effect of TSN IIA on TGF beta1 and Smads signal pathway in local myocardium."

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"Consistent with these reports, we found that TGF-beta1 could up-regulate the protein expression of TGF-beta RI, TGF-beta RII, p-Smad2 and p-Smad3."

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"TGFbeta1 induced alpha-SMA expression was reduced by MEK inhibition (U0126); however, the levels of pERK, pSmad3, or the extent of the interaction between pSmad3 and CBP induced by TGFbeta1 were not affected by FSK."

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"TGF-beta1 caused upregulation of smad3 and p-smad3 expressions, while decreased smad7 expression."

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"Both SFRP1 and FRZB inhibit the TGFbeta1 induced increase of active beta-catenin, but do not influence the TGFbeta1 induced phosphorylation levels of SMAD3, positioning Wnt signaling activity downstream of the active TGFbeta signal in lung fibroblasts, but not in alveolar epithelial cells."

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"For the expression of Smad3, the OGD group had significantly higher level of Smad3 than the control group, and transfection of TGF-beta1 or Smad3 further up-regulated the Smad3 expression (P < 0.05, XREF_FIG)."

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"Following transfection of A549 cells with miR-320a-3p mimic, the expression of p-SMAD3 induced by TGF-β1 was significantly reduced, while total SMAD3 was unaffected ( xref )."