IndraLab

Statements


TGFB1 activates SMAD2. 23 / 23
13 10 |

"Blocking TGF-beta1 signaling pathway by knocking down Smad2 significantly blunted the aldosterone induced fibronectin production."

"FIGURE 11. TGF-beta1 induces activation of Smad2/3 pathway in AML12 cell line"

"TGFb1 signaling activates receptor SMADs, SMAD2 and SMAD3, which associate with a variety of nuclear factors to regulate gene transcription"

"TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, was also suppressed by VEGF. VEGF attenuation of TGF-beta action was also demonstrated in two other endothelial cell lines. In conclusion, VEGF attenuates TGF-beta action in the human endothelial cell, specifically at the level of transcription of PAI-1 gene and Smad2/3 phosphorylation"

"Both SMAD2 and SMAD1/5 were activated upon exposure to TGF-beta1"

"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."

"Expression of wild-type Dab2 in a TGFbeta-signaling mutant restores TGFbeta-mediated Smad2 phosphorylation, Smad translocation to the nucleus and Smad-dependent transcriptional responses."

"Expression of wild-type Dab2 in a TGFbeta-signaling mutant restores TGFbeta-mediated Smad2 phosphorylation, Smad translocation to the nucleus and Smad-dependent transcriptional responses."

"TGF-beta phosphorylation of Smad2/3, an obligatory step of intracellular TGF-beta signaling, was also suppressed by VEGF. VEGF attenuation of TGF-beta action was also demonstrated in two other endothelial cell lines. In conclusion, VEGF attenuates TGF-beta action in the human endothelial cell, specifically at the level of transcription of PAI-1 gene and Smad2/3 phosphorylation"

"In this study, we generated T cell-specific Smad2 conditional knockout (KO) mice and unexpectedly found that Smad2 and Smad3 were redundantly essential for TGF-beta-mediated induction of Foxp3-expressing regulatory T cells and suppression of IFN-gamma production in CD4(+) T cells."

"In our previous studies we have shown that both Smad2 and p38 MAPK were activated in human lung fibroblasts within 10 min of TGF1 stimulation, and peak activation was reached at 1 h (19)."

"Primary astrocytes cultured from SBE-luc mice showed specific activation of the reporter in response to Smad2/3-activating TGF-beta family members. Treatment of mice with the endotoxin LPS resulted in a fast and vigorous, but transient activation of the reporter in the intestine"

"The changes in glucocorticoid binding were associated with identical changes in GR protein and mRNA levels Functional inactivation of Smad 2/3 and AP-1 limited the response to TGF-beta 1, indicating a role for these transcription factors TGF-beta 1 increases glucocorticoid binding and signaling in inflammatory cells through a Smad 2/3- and AP-1-mediated process"

"TGFb1 signaling activates receptor SMADs, SMAD2 and SMAD3, which associate with a variety of nuclear factors to regulate gene transcription"

"Blocking TGF-beta1 signaling pathway by knocking down Smad2 significantly blunted the aldosterone induced fibronectin production. "

"Both SMAD2 and SMAD1/5 were activated upon exposure to TGF-beta1"

"The changes in glucocorticoid binding were associated with identical changes in GR protein and mRNA levels Functional inactivation of Smad 2/3 and AP-1 limited the response to TGF-beta 1, indicating a role for these transcription factors TGF-beta 1 increases glucocorticoid binding and signaling in inflammatory cells through a Smad 2/3- and AP-1-mediated process"

"Modified assertion"

"In this study, we generated T cell-specific Smad2 conditional knockout (KO) mice and unexpectedly found that Smad2 and Smad3 were redundantly essential for TGF-beta-mediated induction of Foxp3-expressing regulatory T cells and suppression of IFN-gamma production in CD4(+) T cells."

"Modified assertion"

"By RT-PCR we have shown that TGFbeta up-regulates expression not only of plasminogen activator inhibitor type-1 (PAI-1), but also of the urokinase-type plasminogen activator receptor (uPAR), whose inhibition by specific antibodies blunted the TGFbeta angiogenic response in vitro. The SMAD2/3 and FAK signaling pathways were activated by TGFbeta in MVEC"

"In our previous studies we have shown that both Smad2 and p38 MAPK were activated in human lung fibroblasts within 10 min of TGF1 stimulation, and peak activation was reached at 1 h (19)."

"By RT-PCR we have shown that TGFbeta up-regulates expression not only of plasminogen activator inhibitor type-1 (PAI-1), but also of the urokinase-type plasminogen activator receptor (uPAR), whose inhibition by specific antibodies blunted the TGFbeta angiogenic response in vitro. The SMAD2/3 and FAK signaling pathways were activated by TGFbeta in MVEC"