IndraLab

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TGFB1 increases the amount of TGFBR1. 24 / 24
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"Upon pretreatment of the cells with TGF-beta led to the activation of TGFBR1."
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"Based on current research, we hypothesise that EDPs and TGF-beta1 released by elastic fibre degradation under high glycaemic condition in vessels can lead to increased ELR-1, ALK-5 and PKCbetaII expression in SMCs and lead to osteogenic transformation of SMCs."
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"TbetaRI expression in other mutant clone (SNU-620-mt Smad4-2) was not increased by TGF-beta1 treatment (data not shown)."
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"Next, we measured genes involved in LC differentiation and discovered that BMP7, but not TGF-beta1, was able to up-regulate the expression of ALK3 and ALK5, the receptors of BMP7 (ALK3) and TGF-beta1 (ALK5 and ALK3)."
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"Expression of microglial TbetaR-I was upregulated by TGF-beta1."
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"Protein levels of TbetaRI increased after activation by TGF-beta1, while TbetaRII expression levels were not obviously increased."
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"TGF-beta1 induced up-regulation of both Tgf-b1 and Tgf-br1 expression whereas inhibition of TGF-beta1 signaling in the TGF-beta1 + SB525334 resulted in significant downregulation of both Tgf-b1 and Tgf-br1 at day 3 and whereas at day 5, Tgf-b1 was still downregulated both not its receptor, Tgf-br1."
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"Importantly, the inhibitor of beta-catenin (ICG-001) suppressed TGFbeta1- and TGFbeta2 induced ALK5 expression in both normal and Akt1 deficient HMECs indicating the integral role of Akt1-beta-catenin pathway in the regulation of ALK5 expression promoting EndMT."
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"Both TGF-beta1 and TGF-beta3 increased Tgfbr1 expression in a dose dependent manner, see XREF_FIG (N = 3, * P < = 0.01)."
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"Compared with the control group, TbetaRI and TbetaRII expression was significantly increased by TGF-beta 1 -stimulation."
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"The expression level of the TGF-beta receptor TGFBR1 was increased 2.9-fold by TGF-beta1 treatment and reduced to 79% by AM251 (XREF_FIG)."
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"To better understand the role of the sex hormones in the TGF-β1 system, we investigated whether DHT and estradiol affect the TGF-β1-induced expression of the receptors TGFBR1 and TGFBR2 ( xref )."
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"TbetaRI and TbetaRII expression was significantly increased by TGF-beta 1 -stimulation compared with the control group."
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"Similar to the control siRNA and sham plasmid, Arkadia siRNA did not significantly affect the expression of TbetaRI, but lactacystin inhibited the expression of TbetaRI induced by TGF-beta 1 in HKCs."
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"CASE treatment (40 and 80 microg/ml) significantly decreased the TGF-beta 1 -induced elevation in TbetaRI and TbetaRII expression in a dose dependent manner compared with the TGF-beta 1 group."
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"The finding that TGFbeta1 treatment increased Tgfbr1 and Tgfbr2 expression suggests an increased capacity for autocrine anti-inflammatory signaling, which was not the case for IL-10 treatment."
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"TGF-beta1 treatment increased the level of ALK5 transcription, which was decreased upon co-treatment with eupatolide in a time dependent manner."
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"(1) TGF-beta1, in a concentration dependent manner, upregulated ALK5 and PAI-1 expressions in the HTFs, which peaked between 24 and 36 h."
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"In cultured HK-2 cells, TGF-beta1 dramatically up-regulated TbetaRI expression and phosphorylated levels of Smad 2 and Smad 3, but down-regulated Smad7 expression, consistent with the data in vivo, and confirmed the characteristics of TGF-beta and Smads signaling in EMT [XREF_BIBR]."
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"TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture."
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"Collectively, these data demonstrate that the profibrogenic effects of TXNDC5 were mediated through increased TGFbeta1 signaling activity via increased TGFBR1 expression levels."
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"In accord with previous studies, TGF-beta1 stimulated the expression of TGFR1 while suppressing TGFR2 expression (XREF_FIG)."
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"They also demonstrate that Chit1 is an important TGF-beta1 cofactor that enhances TGFR1 and TGFR2 expression, as well as canonical and noncanonical TGF-beta1 signaling."
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"Although our findings are not completely exhaustive, indicate that ALK-5 expression is upregulated by exogenous TGFbeta1 treatment, but that the downstream activation of signal transduction, through the ALK-5 receptor, may depend on alphavbeta3 mediated release of endogenous TGFbeta1."
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