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SLC22A3 — TGFBR1

Text-mined interactions from Literome

Bakin et al., J Cell Sci 2002 (Cell Transformation, Neoplastic) : Expression of TGFbeta type II ( TbetaRII ) and type I ( TbetaRI/Alk5 ) kinase-inactive receptors blocked EMT and activation of p38MAPK, whereas expression of constitutively active Alk5-T204D resulted in EMT and phosphorylation of MKK3/6 and p38MAPK
Valcourt et al., Mol Biol Cell 2005 : Using a TGF-beta type I receptor that can not activate Smads nor induce EMT , we found that Smad signaling is critical for regulation of all tested gene targets during EMT
Desgrosellier et al., Dev Biol 2005 : Smad6, an inhibitor of Smad signaling downstream of ALK2, but not ALK5 , inhibited EMT in AV cushion endocardial cells
Townsend et al., J Biol Chem 2008 : Here we show that the Type I TGFbeta receptor ALK5 is required for endocardial cell EMT
Liu et al., Cell Motil Cytoskeleton 2008 (Fibrosis...) : Suppression of TbetaR-I , Smad2 or Smad3 by siRNA partially blocks EMT induction by cytomix plus TGF-beta1, indicating cytomix augments TGF-beta1 induced EMT through enhancing TbetaR-I and Smad signaling
Park et al., Cancer Sci 2011 (Cell Transformation, Neoplastic...) : The novel ALK5 inhibitor, EW-7203, efficiently inhibited TGF-ß1 induced Smad signalling, EMT and breast tumor metastasis to the lung in vivo, demonstrating that EW-7203 has therapeutic potential for breast cancer metastasis to the lung