Gene interactions and pathways from curated databases and text-mining

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TGFB1 — TGFBR2

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

Kleeff et al., Pancreas 1999 (Pancreatic Neoplasms) : We conclude that the TGF-beta 1-induced T beta RII upregulation serves to enhance TGF-beta 1 responsiveness in COLO-357 cells, and that this upregulation requires the presence of adequate levels of T beta RI and T beta RII , and a functional Smad4 gene product
Zhao et al., Mol Cell Endocrinol 1999 : Co-expression with TbetaRII was required for binding and cross linking of TGF-beta1 to TbetaRI deltaK
Ripley et al., Gynecol Oncol 2001 (Endometrial Neoplasms) : GM-CSF and TGF-beta1 regulate their own expression and the expression of TGF-beta type II receptor , which were both upregulated by 17beta-estradiol and medroxyprogesterone acetate treatment and reversed following cotreatment with their respective receptor antagonists
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
Fernandez et al., J Exp Med 2002 (Plasmacytoma) : Disruption of the expression of TGF-beta1 by antisense TGF-beta1 mRNA restores localization of TbetaRII at the PCT cell surface, indicating a ligand induced impediment in receptor trafficking
Chen et al., Biochem J 2002 : In summary, this report demonstrated that acetaldehyde stimulated TGF-beta signalling by increasing the secretion and activation of latent TGF-beta1 as well as by inducing the expression of Tbeta-RII in cultured HSC
Lu et al., Zhonghua Shao Shang Za Zhi 2004 (Cicatrix, Hypertrophic) : The mRNA expressions of TGF beta 1 , TGF beta 2 and TGFRI were evidently increased with decreased mRNA expression of TGF-beta 3 and TGFR II in the hypertrophic scar when compared with those in the normal skin
Huo et al., Cell Biol Toxicol 2007 (MAP Kinase Signaling System) : Activation of extracellular signal regulated kinase by TGF-beta1 via TbetaRII and Smad7 dependent mechanisms in human bronchial epithelial BEP2D cells
Vásquez et al., J Cell Physiol 2007 : High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC
Zhu et al., Prostate 2008 (Neoplasms, Hormone-Dependent...) : TGF-beta1 induced transcriptional activity enhanced by DHT in both cell lines ( LNCaP-TbetaRII and PC-3-AR ) via AR-Smad4 interaction
Vega et al., Cardiovasc Res 2009 (Pregnancy Complications) : hENT1 is down-regulated by activation of TbetaRII by TGF-beta1 in HUVECs, a phenomenon where NO and Sp1 play key roles
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
Boudreau et al., J Virol 2009 : Furthermore, the human Nox4 promoter was responsive to TGF-beta1 , and the HCV core dependent induction of Nox4 was blocked by antibody against TGF-beta or the expression of dominant negative TGF-beta receptor type II
Imamura et al., Atherosclerosis 2010 : EPCs expressed TGF-beta receptor type II ( TGF-beta RII ) and TGF-beta1 induced the phosphorylation of Smad 2 in EPCs
Li et al., J Cell Biochem 2012 : We thus conclude that miR-17-92 cluster could inhibit TGFB pathway induced proliferation inhibition and collagen synthesis in PMCs by directly targeting TGFBR2 , SMAD2, and SMAD4
Inagaki et al., Cell Struct Funct 1994 (Carcinoma, Hepatocellular...) : We report that TGF-beta 1 protein selectively increased steady-state levels of the mRNA for the serine/threonine kinase receptor 1 ( SKR1 ), a member of the TGF-beta superfamily receptor genes in these cells, whereas TGF-beta 1 had little effect on expression of the TGF-beta receptor type II gene
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
Ward et al., Atherosclerosis 1998 (Arterial Occlusive Diseases...) : Tranilast also prevented the PDGF-BB induced increases in TbetaRII but only partially inhibited the TGF-beta1 induced upregulation of TbetaRII
Sarkar et al., Endocrinology 1998 : Furthermore, the TGF-beta1 gene-transcription response is less dependent on TbetaR-II receptor expression than is the TGF-beta1 growth-inhibitory response