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TGFB1 activates SMAD3. 9 / 338
| 5 94 178
sparser
"Additionally, as shown in C, reporter assay analysis with SBE-Luc, which includes Smad binding elements (SBE), verified that the transcriptional activation of Smad2 and Smad3 by TGF-β1 appeared to be [MISSING/INVALID API KEY: limited to 200 char for Elsevier]"
sparser
"Inhibition of JNK1 activation prevents TGF-β1-induced Smad3 activation and nuclear translocation ( xref )."
reach
"The results demonstrated that the transcription of all three Smads increased in TGF-beta1-treated LX-2 cells; however, AdNDRG2 only attenuated the increase in Smad3 induced by TGF-beta1, while Smad2 and Smad7 showed no differences among compared groups (XREF_FIG)."
reach
"The activation of smad3 by TGF-beta1 was closely associated with the induction of FN, MMP-2, and MMP-9 expression."
sparser
"Disruption of the primary cilium inhibits TGFβ1-induced activation of SMAD3."
sparser
"It has been reported recently that TGFβ1-activated transcription factors Smad3 and Smad4 specifically interact with HNF4α and inhibit HNF4α trans -activating activity [ xref , xref ]."
reach
"Furthermore, we show that the cilium mediates this response through distinct spatial localisation of TGFbeta receptors and signalling components at the primary cilium, whereby TGFbeta1 mediated activation of SMAD3 takes place at the ciliary base."
reach
"Using the ROS osteoblast like cells, we demonstrated that TGF-beta1 activates Smad2 and Smad3 at the conserved TGF-beta receptor phosphorylation motif (SSXS) and the nuclear accumulation of activated Smad2 and Smad3 occurs in a time dependent fashion."
sparser
"That 500 nmol/L LDN-193189 weakly blocked activation of Smad3 by TGF-β1 ( xref ), suggested that activation of Smad3 by rapamycin is dependent on the kinase activity of a BMP type I receptor."
TGFB1 activates SMAD3. 10 / 38
24 14 |
bel
"Previously we have reported that the intracellular effectors of TGF-beta, Smad3 and Smad4, functionally cooperate with Sp1 to activate the human p21 promoter in hepatoma HepG2 cells."
bel
"Transforming growth factor-beta (TGF-beta) is a potent inhibitor of skeletal muscle differentiation, but the molecular mechanism and signaling events that lead to this inhibition are poorly characterized. Here we show that the TGF-beta intracellular effector Smad3, but not Smad2, mediates the inhibition of myogenic differentiation in MyoD-expressing C3H10T1/2 cells and C2C12 myoblasts by repressing the activity of the MyoD family of transcriptional factors. Central to the induction of myogenic differentiation is the function of the MyoD family of basic helix-loop-helix (bHLH) transcription factors, which include MyoD, myogenin, Myf5, and MRF4 and are collectively referred to as myogenic regulatory factors or MRFs"
bel
"TGFb1 signaling activates receptor SMADs, SMAD2 and SMAD3, which associate with a variety of nuclear factors to regulate gene transcription"
bel
"TGF-beta1 (1 ng/ml) significantly upregulated SMAD phosphorylation in COPD ASMC following 2-h stimulation (P < 0.05; n = 5; Fig. 4A); however, the differences were not significant for other ASMC types."
bel
"The expression of JunD colocalised with pSmad 3 in fibrotic skin and silencing of Smad 3 or Smad 4 by siRNA prevented the induction of JunD by TGFbeta......The expression of JunD was analysed by real-time PCR, immunofluorescence, western blotting and immunohistochemistry. "
bel
"However, Western blot analysis reveals that IGF-I selectively inhibits the TGF-beta-triggered activation Smad3 but not Smad2, while not altering expression of total Smads 2, 3, or 4. The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY29004 reverses the ability of IGF-I to inhibit TGF-beta-induced transcriptional responses and the activation of Smad3, suggesting that the suppression of TGF-beta signaling by IGF-I is mediated through activation of PI3K. Moreover, we show that enforced expression of dominant-negative PI3K (DN-p85alpha) or phosphatidylinositol 3-phosphate-phosphatase, PTEN, also reverse the suppressive effect of IGF-I on TGF-beta-induced 3TP-luciferase reporter activity, whereas constitutively active PI3K (p110alphaCAAX) completely blocks TGF-beta-induced 3TP-luciferase reporter activity."
bel
"A recent study [22] provided evidence for the contribution of Smad1, in addition to Smad3, to TGF-bdependent stimulation of collagen and CCN2 genes in cultured dermal fibroblasts."
bel
"Furthermore, expression of dominant negative Smad3 or Smad4 in cells decreased or abolished the stimulation of beta(5) promoter activity by TGF-beta. Smad4 mutant also inhibited the up-regulation of surface beta(5) level by TGF-beta. Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors."
bel
"TGFb1 signaling activates receptor SMADs, SMAD2 and SMAD3, which associate with a variety of nuclear factors to regulate gene transcription"
bel
"These result suggest that TGF-beta1 stimulation of VEGF production by fibroblasts is regulated by Smad3 but not by Smad2 signaling"
TGFB1 activates phosphorylated SMAD3. 4 / 4
| 4
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"UDCA-LPE also decreased phosphorylated Smad3 and Smad2 directly induced by TGF-beta1."
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"In XREF_FIG, phosphorylated Smad3 was assessed by Western blotting on fibroblasts treated with TGF-beta 1 with and without rapamycin."
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"Importantly, we found that the nuclear translocation of phosphorylated Smad3 induced by TGF-beta1 could be maintained only under Kindlin-1 overexpression, suggesting that Kindlin-1 is required for the nuclear translocation of phosphorylated Smad3."
reach
"Therefore, we suggest that in the cytoplasm, phosphorylated Smad3 induced by TGF-beta1 stimulation increases binding to NFI-C, and results in the degradation of NFI-C."
TGFB1 bound to its activates SMAD3. 2 / 2
| 2
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"Once activated, TGF-beta1 binds its receptors and then activates its downstream signaling mediators of Smad3, to exert its biological activities [XREF_BIBR - XREF_BIBR]."
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"It is now clear that after binding to its receptors, TGF-beta1 activates its downstream signaling pathway, Smad 2 and Smad3, to mediate fibrosis, which is negatively regulated by Smad7, an inhibitor of TGF-beta signaling, via the ubiquitin-proteasome degradation mechanism XREF_BIBR, XREF_BIBR."