IndraLab
Statements
"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"
"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"
"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"
"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"
"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"
"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"