IndraLab

Statements


TGFB1 increases the amount of TGFBR1. 10 / 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."
TGFB1 bound to TGFBR2 increases the amount of TGFBR1 bound to TGFBR2. 1 / 1
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"from Figure 1 - Fig 1. The transforming growth factor beta (TGF-b) signaling pathway. TGF-b binds type II TGF-b receptor (TbRII), directly or through TbRIII, inducing association of TbRII with TbRI. TbRII then phosphorylates and activates TbRI, which then phosphorylates Smad2 or Smad3. Phosphorylated Smad2 or Smad3 associates with Smad4 and they translocate into the nucleus, where they activate transcription of target genes. Smad7 inhibits TGF-b signaling by preventing the activation of Smad2 or Smad3 by TbRI."
TGFB1 bound to TGFBR2 and TGFBR3 increases the amount of TGFBR1 bound to TGFBR2. 1 / 1
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"from Figure 1 - Fig 1. The transforming growth factor beta (TGF-b) signaling pathway. TGF-b binds type II TGF-b receptor (TbRII), directly or through TbRIII, inducing association of TbRII with TbRI. TbRII then phosphorylates and activates TbRI, which then phosphorylates Smad2 or Smad3. Phosphorylated Smad2 or Smad3 associates with Smad4 and they translocate into the nucleus, where they activate transcription of target genes. Smad7 inhibits TGF-b signaling by preventing the activation of Smad2 or Smad3 by TbRI."