gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Transforming growth factor, beta receptor 1

TGF-beta type I receptor, ALK5, TbetaRI, TGFBR1
The protein encoded by this gene forms a heteromeric complex with type II TGF-beta receptors when bound to TGF-beta, transducing the TGF-beta signal from the cell surface to the cytoplasm. The encoded protein is a serine/threonine protein kinase. Mutations in this gene have been associated with Loeys-Dietz aortic aneurysm syndrome (LDAS). Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2008] (from NCBI)
Top mentioned proteins: TGF-beta, Smad2, TGF-beta type II receptor, Smad3, V1a
Papers using TGF-beta type I receptor antibodies
The Heidelberg classification of renal cell tumours.
Yeudall Andrew, In PLoS ONE, 1996
... Cells were treated with 2 µM TGFBR1 inhibitor (SB431542, Sigma Aldrich, Munich, Germany), 10 µM ...
Papers on TGF-beta type I receptor
FGF-2 inhibits Endothelial-Mesenchymal Transition through microRNA-20a-mediated repression of canonical TGF-β Signaling.
Krenning et al., Groningen, Netherlands. In J Cell Sci, Feb 2016
We identified ALK5, TGFBR2 and SARA as direct miR-20a targets.
Galangin inhibits hypertrophic scar formation via ALK5/Smad2/3 signaling pathway.
Li et al., Shanghai, China. In Mol Cell Biochem, Feb 2016
Such bioactivity of galangin resulted from its selective targeting to the activin receptor-like kinase 5 (ALK5) was demonstrated by ALK5 knockdown and over-expression experiments.
Rho GTPase Signaling Promotes Constitutive Expression and Release of TGF-β2 by Human Trabecular Meshwork Cells.
Stubbs et al., United States. In Exp Eye Res, Jan 2016
By comparison, perfusing segments with a TGFβRI/ALK-5 antagonist (SB-431542) unexpectedly elicited a significant and sustained increase in outflow facility, implicating a role for TM-localized constitutive expression and release of TGF-β2.
Identification of Top-ranked Proteins within a Directional Protein Interaction Network using the PageRank Algorithm: Applications in Humans and Plants.
Du et al., Fredericton, Canada. In Curr Issues Mol Biol, Jan 2016
Eight proteins (ACVR1, CDC42, RAC1, RAF1, RHOA, TGFBR1, TRAF2, and TRAF6) are ranked in the top 50 key players in both signal emission and signal reception and in interaction with many other proteins.
Arterial tortuosity in genetic arteriopathies.
Morris, Houston, United States. In Curr Opin Cardiol, Nov 2015
RECENT FINDINGS: Although arterial tortuosity has been primarily described in Loeys-Dietz syndrome due to TGFBR1 and TGFBR2 mutations and in arterial tortuosity syndrome due to SLC210A mutations, recent studies that use quantitative measures of tortuosity suggest that tortuosity is present in many other genetic conditions associated with aortic dilation and dissection.
Genetics of hereditary large vessel diseases.
Morisaki et al., Ōsaka, Japan. In J Hum Genet, Nov 2015
Genes identified for these diseases include FBN1, TGFBR1, TGFBR2, SMAD3, TGFB2, TGFB3, SKI, EFEMP2, COL3A1, FLNA, ACTA2, MYH11, MYLK and SLC2A10, as well as others.
The TGF-β Signaling Regulator PMEPA1 Suppresses Prostate Cancer Metastases to Bone.
Guise et al., Indianapolis, United States. In Cancer Cell, Jul 2015
Our study reveals that the TGFBR1 inhibitor SD208 effectively reduces prostate cancer bone metastases.
Activin Receptor-Like Kinase Receptors ALK5 and ALK1 Are Both Required for TGFβ-Induced Chondrogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells.
van der Kraan et al., Nijmegen, Netherlands. In Plos One, 2014
Transforming Growth Factor β (TGFβ) is crucial for inducing chondrogenic differentiation of BMSCs and is known to signal via Activin receptor-Like Kinase (ALK) receptors ALK5 and ALK1.
TGFβ isoforms and receptors mRNA expression in breast tumours: prognostic value and clinical implications.
Vitetta et al., Brisbane, Australia. In Bmc Cancer, 2014
METHODS: The mRNA levels of TGFB1, TGFB2, TGFB3, TGFBR1 and TGFBR2 were analysed in primary breast tumours and adjacent normal breast tissues, and the associations with tumour characteristics and patients' overall and relapse-free survival were evaluated, using the public gene expression microarray data from The Cancer Genome Atlas (n = 520) and the Gene Expression Omnibus (four datasets) and our quantitative real-time PCR validation data (n = 71).
Digenic/multilocus aetiology of multiple self-healing squamous epithelioma (Ferguson-Smith disease): TGFBR1 and a second linked locus.
Goudie et al., Dundee, United Kingdom. In Int J Biochem Cell Biol, 2014
We review here the investigations leading to the discovery of loss of function mutations in TGFBR1 that are responsible for the disease.
TGFBR1 and cancer susceptibility.
Wang et al., Winston-Salem, United States. In Trans Am Clin Climatol Assoc, 2013
TGFBR1 6A is a polymorphism consisting of a 9-base pair in-frame deletion within exon 1 of the type I TGF-β receptor (TGFBR1), which results in a receptor with decreased TGF-β signaling capability.
Seven new loci associated with age-related macular degeneration.
AMD Gene Consortium et al., Regensburg, Germany. In Nat Genet, 2013
Our results include seven loci with associations reaching P < 5 × 10(-8) for the first time, near the genes COL8A1-FILIP1L, IER3-DDR1, SLC16A8, TGFBR1, RAD51B, ADAMTS9 and B3GALTL.
Dependency of colorectal cancer on a TGF-β-driven program in stromal cells for metastasis initiation.
Batlle et al., Barcelona, Spain. In Cancer Cell, 2012
The activity of TGF-β on stromal cells increases the efficiency of organ colonization by CRC cells, whereas mice treated with a pharmacological inhibitor of TGFBR1 are resilient to metastasis formation.
An inhibitor of transforming growth factor beta type I receptor ameliorates muscle atrophy in a mouse model of caveolin 3-deficient muscular dystrophy.
Sunada et al., Okayama, Japan. In Lab Invest, 2012
We show that a TbetaRI kinase inhibitor, Ki26894, restores impaired myoblast differentiation in vitro caused by activin, myostatin, and TGF-beta1, as well as CAV3(P104L).
Post-translational regulation of TGF-β receptor and Smad signaling.
Derynck et al., San Francisco, United States. In Febs Lett, 2012
TGF-beta family signaling through Smads is conceptually a simple and linear signaling pathway, driven by sequential phosphorylation, with type II receptors activating type I receptors, which in turn activate R-Smads [review]
Structural studies of the TGF-βs and their receptors - insights into evolution of the TGF-β superfamily.
Hinck, San Antonio, United States. In Febs Lett, 2012
analysis of evolution of the TGF-beta superfamily and how they signal through a single pair of receptors, known as TbetaR-I and TbetaR-II [review]
USP4 is regulated by AKT phosphorylation and directly deubiquitylates TGF-β type I receptor.
ten Dijke et al., Leiden, Netherlands. In Nat Cell Biol, 2012
Results uncover USP4 as an important determinant for crosstalk between TGF-beta/TGF-beta type I receptor and AKT signalling pathways.
Involvement of transforming growth factor β and its type 1 receptor in the development of breast cancer.
Bereschanskaya et al., Moscow, Russia. In Bull Exp Biol Med, 2011
several polymorphisms detected in the TGFbeta1 gene and its receptor associated with benign and malignant breast tumors
Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1.
Lane et al., Dundee, United Kingdom. In Nat Genet, 2011
dideoxy sequencing of TGFBR1 identified 11 distinct monoallelic mutations in 18 affected families with multiple self-healing squamous epithelioma
TGF-beta1-induced migration of bone mesenchymal stem cells couples bone resorption with formation.
Cao et al., Birmingham, United States. In Nat Med, 2009
Treatment with a TGF-beta type I receptor inhibitor partially rescued the uncoupled bone remodeling and prevented the fractures.
share on facebooktweetadd +1mail to friends