Gene interactions and pathways from curated databases and text-mining

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Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Luo et al., Mol Cell Proteomics 2006 : Endogenous transforming growth factor-beta receptor mediated Smad signaling complexes analyzed by mass spectrometry
Shinto et al., Cancer Sci 2010 (Lymphatic Metastasis...) : A novel TbetaR-I kinase inhibitor, Ki26894, inhibits the phosphorylation of Smad2 at the ATP binding site of TbetaR-I
Sun et al., Nucleic Acids Res 2006 : RBPMS interacts with TGF-beta receptor type I (TbetaR-I) , increases phosphorylation of C-terminal SSXS regions in Smad2 and Smad3, and promotes the nuclear accumulation of the Smad proteins
Carvalho et al., J Cell Sci 2007 : This again caused defects in the yolk sac vasculature with embryonic lethality at E10.5, demonstrating that TGFbeta/ALK1 signalling in ECs can not compensate for the lack of TGFbeta/ALK5 induced SMAD2/3 signalling in vivo
Jeon et al., J Cell Sci 2006 : In addition, SPC increased secretion of TGF-beta1 through an ERK dependent pathway, and the SPC induced expression of alpha-SMA and delayed phosphorylation of Smad2 were blocked by SB-431542, a TGF-beta type I receptor kinase inhibitor, or anti-TGF-beta1 neutralizing antibody
Schniewind et al., Oncogene 2007 (Adenocarcinoma...) : Ectopic expression of dominant negative mutants of the TGF-beta type II receptor or type I receptor/activin receptor-like kinase 5 (ALK5) in TGF-beta-sensitive pancreatic ductal adenocarcinoma PANC-1 cells prevented the TGF-beta induced activation of transfected Smad-responsive reporter genes and growth arrest ... The growth-inhibitory effect was mimicked by stable expression of kinase-active ALK5 ( ALK5-T204D ), and was dependent on ALK5 's ability to activate Smad signaling, as a ALK5 derived mutant with an intact kinase domain but deficient in its ability to activate Smads ( RImL45 ) failed to suppress proliferation in the absence of added TGF-beta
Xie et al., Am J Physiol Cell Physiol 2011 : Mechanistically, Cav-2 inhibits anti-proliferative action of TGF-ß by suppressing Alk5-Smad2/3 pathway manifested by reduced magnitude and length of TGF-ß induced Smad2/3 phosphorylation as well as activation of activin receptor-like kinase-5 (Alk5)-Smad2/3 target genes plasminogen activator inhibitor-1 and collagen type I in Cav-2 positive ECs
Ishida et al., J Invest Dermatol 2006 (Scleroderma, Systemic) : Taken together, these results indicate that SM305 inhibits intracellular TGF-beta signaling through selective interference with ALK5 mediated Smad activation, resulting in marked suppression of profibrotic responses induced by TGF-beta in vivo and in vitro
Verschueren et al., J Biol Chem 1999 : Activation of transforming growth factor beta receptors causes the phosphorylation and nuclear translocation of Smad proteins, which then participate in the regulation of expression of target genes
Imamichi et al., Biol Chem 2005 : In contrast, ALK5 inhibition effectively blocked Smad2 phosphorylation
Tian et al., Cancer Res 2004 (Breast Neoplasms...) : Our present data based on selective interference with activation of endogenous Smad2 and Smad3 by stable expression of a mutant form of the TGF-beta type I receptor ( RImL45 ) unable to bind Smad2/3 but with a functional kinase again show that reduction in Smad2/3 signaling by expression of RImL45 enhanced the malignancy of xenografted tumors of the well differentiated MCF10A derived tumor cell line MCF10CA1h, resulting in formation of larger tumors with a higher proliferative index and more malignant histologic features
Rudini et al., EMBO J 2008 : ECs lacking VE-cadherin are less responsive to TGF-beta/ALK1- and TGF-beta/ALK5 induced Smad phosphorylation and target gene transcription
Yakymovych et al., J Biol Chem 2004 : Here we show that substitutions of Arg-462 and Cys-463 residues, which are in proximity of the C-terminal serine residues, inhibited TGFbeta type I receptor dependent phosphorylation of the C-terminal Smad2 peptides and full-length GST-Smad2 proteins in vitro
Ungefroren et al., Int J Oncol 2011 (Carcinoma, Pancreatic Ductal...) : Biochemically, dnSrc inhibition failed to block TGF-ß1/ALK5 induced activation of Smad2 and Smad3, but partially inhibited transcriptional activation of TGF-ß/Smad-responsive reporter genes, and effectively blocked basal and TGF-ß1 induced activation of p38 MAPK
Li et al., Eur J Pharmacol 2009 : In vitro, NDGA inhibited TGF-beta type I receptor mediated Smad2 phosphorylation in crude cell lysates and in a purified preparation
Moonen et al., Cardiovasc Res 2010 : TGFbeta1-driven EndMT is mediated by ALK5 kinase activity, increased downstream Smad2 signalling, and reduced protein levels of inhibitor of DNA binding protein 3
Abdollah et al., J Biol Chem 1997 : TbetaRI phosphorylation of Smad2 on Ser465 and Ser467 is required for Smad2-Smad4 complex formation and 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
Kondo et al., Cancer Sci 2004 : Smad3D407E was not phosphorylated by the constitutively active form of the TGF-beta type I receptor , and inhibited the phosphorylation of co-expressed wild-type Smad2 and Smad3
van der Kraan et al., Cell Tissue Res 2012 (Fibrosis...) : Transforming growth factor-ß has recently been demonstrated to signal not only via activin receptor-like kinase 5 (ALK5) induced Smad2/3 phosphorylation, but also via ALK1 induced Smad1/5/8 phosphorylation in articular cartilage
Shinto et al., Br J Cancer 2010 (Adenocarcinoma, Scirrhous...) : A TbetaR type I (TbetaR-I) kinase inhibitor, Ki26894, inhibits the phosphorylation of Smad2 at an ATP binding site of TbetaR-I