◀ Back to SLC22A3

SLC22A3 — SMAD4

Text-mined interactions from Literome

Rhyu et al., J Am Soc Nephrol 2005 (Fibrosis...) : Phosphorylation of Smad proteins and/or mitogen activated protein kinases ( MAPK ) is required for TGF-beta1 induced EMT
Valcourt et al., Mol Biol Cell 2005 : Ectopic Smad2 or Smad3 together with Smad4 enhanced, whereas dominant negative forms of Smad2, Smad3, or Smad4 , and wild-type inhibitory Smad7, blocked TGF-beta induced 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
Liu et al., Perit Dial Int 2008 (Fibrosis...) : Phosphorylation of Smad proteins is required for TGFbeta1 induced EMT
Miyazono et al., Proc Jpn Acad Ser B Phys Biol Sci 2009 (Disease Progression...) : Multiple transcription factors, including deltaEF1/ZEB1, SIP1/ZEB2, and Snail/SNAI1, are induced by TGF-beta-Smad signaling and play critical roles in TGF-beta induced EMT ... In addition, both non-Smad signaling activated by TGF-beta and cross-talk with other signaling pathways play important roles in induction of EMT
Zhou et al., J Am Soc Nephrol 2010 : Because Smad proteins transduce TGF-beta signaling from the cytosol to the nucleus and HSP72 assists in protein folding and facilitates nuclear translocation, we investigated whether HSP72 inhibits TGF-beta induced EMT by modulating Smad expression, activation, and nuclear translocation
Townsend et al., Cells Tissues Organs 2011 : Targeting of Smad4, the common mediator Smad, demonstrated that Smad signaling is required for EMT in the AVC and TGFßR3 dependent EMT stimulated by TGFß2 or BMP-2 ... Taken together, our data demonstrate that TGFßR3 dependent endocardial cell EMT stimulated by either TGFß2 or BMP-2 requires Smad4 and the activation of the Par6/Smurf1 pathway
Hesling et al., EMBO Rep 2011 : Antagonistic regulation of EMT by TIF1? and Smad4 in mammary epithelial cells
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
Ai et al., J Natl Cancer Inst 2011 (Adenocarcinoma...) : Furthermore, high expression of pIgR was sufficient to induce EMT through activation of Smad signaling