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
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
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
Buijs et al., Am J Pathol 2007 (Bone Neoplasms...) : Exogenous addition of BMP7 to human prostate cancer cells dose-dependently inhibited transforming growth factor beta induced activation of nuclear Smad3/4 complexes via ALK5 and induced E-cadherin expression
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
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
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
Abdollah et al., J Biol Chem 1997 : TbetaRI phosphorylation of Smad2 on Ser465 and Ser467 is required for Smad2-Smad4 complex formation and signaling
Ogawa et al., Mol Cell Biochem 2008 : The NF-kappaB p65 and interferon regulatory factor (IRF)-1 induced promoter activity was suppressed by the expression of a constitutively active TGF-beta type I receptor in the presence of Smad3 and Smad4 , which was abrogated by expression of an inhibitory Smad, Smad7