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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to TGFB1

TGFB1 — TGFBR1

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

Piek et al., Int J Cancer 1999 (Glioblastoma...) : Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas
Zieske et al., Invest Ophthalmol Vis Sci 2001 : To determine the effect of epidermal growth factor (EGF) and TGF-beta1 on p15(INK4b) and TbetaR-I and -II expression, human corneal epithelial cells were grown in culture to 50 % to 60 % confluence, and EGF ( 5 ng/ml ) and/or TGF-beta1 ( 2 ng/ml ) were added for 6 hours ... In cultured cells, EGF and TGF-beta1 stimulated TbetaR-II ; however, neither one stimulated TbetaR-I expression
Lindstedt et al., FASEB J 2001 : In isolated TbetaRI- and TbetaRII expressing peritoneal macrophages, the activated TGF-beta1 induces the expression of the plasminogen activator inhibitor 1 ( PAI-1 ), whereas in the mast cells, the levels of TbetaRI, TbetaRII, and PAI-1 expression were below detection
Karlsson et al., Physiol Genomics 2005 : Gene expression profiling demonstrates that TGF-beta1 signals exclusively through receptor complexes involving Alk5 and identifies targets of TGF-beta signaling
Birukova et al., FEBS Lett 2005 : Thus, our data demonstrate for the first time direct link between TGF-beta1 mediated activation of ALK5/Smad and EC barrier dysfunction
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
Matsuzaki et al., Hepatology 2007 (Carcinoma, Hepatocellular...) : Conversely, transforming growth factor beta ( TGF-beta ) activates not only TGF-beta type I receptor ( TbetaRI ) but also c-Jun N-terminal kinase (JNK), which convert the mediator Smad3 into two distinctive phosphoisoforms : C-terminally phosphorylated Smad3 ( pSmad3C ) and linker phosphorylated Smad3 ( pSmad3L )
Velasco et al., J Cell Sci 2008 : L- and S-endoglin differentially modulate TGFbeta1 signaling mediated by ALK1 and ALK5 in L6E9 myoblasts
Alfranca et al., Blood 2008 : MT1-MMP dependent transforming growth factor beta ( TGFbeta ) signaling through Alk5 is also required for PGE ( 2 ) -induced endothelial cord formation in vitro, and Alk5 kinase activity is required for PGE ( 2 ) -induced neovascularization in vivo
Lu et al., Am J Physiol Lung Cell Mol Physiol 2009 : Finally, we noted that SMAD1/5 were activated upon ALK5 inhibition in the presence of low levels of TGF-beta1 , an effect associated with enhanced endothelial proliferation
Kim et al., J Biol Chem 2009 : Taken together, our data indicate that TGF-beta1 induced interaction of TbetaRI and TbetaRII triggers dissociation of TAK1 from TbetaRI, and subsequently TAK1 is phosphorylated through TAB1 mediated autophosphorylation and not by the receptor kinase activity of TbetaRI
Li et al., J Biol Chem 2010 : Formation of a stable KLF4-Smad2 complex in the promoter 's Smad-responsive region mediated cooperative TbetaRI promoter transcription in response to TGF-beta1
Souchelnytskyi et al., EMBO J 1996 : We show here that phosphorylation of TbetaR-I at Ser165 is involved in modulation of TGF-beta1 signaling
Persson et al., J Biol Chem 1997 : In the presence of TGF-beta1 , TbetaR-I/BMPR-IB and TbetaR-II/ActR-IIB formed heteromeric complexes with wild-type TbetaR-II and TbetaR-I , respectively, upon stable transfection in mink lung epithelial cell lines
Kleeff et al., J Biol Chem 1998 (Pancreatic Neoplasms) : The protein synthesis inhibitor cycloheximide ( 10 microg/ml ) completely blocked the TGF-beta1 mediated increase in TbetaRI and TbetaRII expression