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Systemic activation of Activin A signaling causes chronic kidney disease-mineral bone disorder. (Review)
TGFbetaR1 rs10739778 was associated with blood pressure in healthy pregnant women.
Treatment of T. cruzi-infected cardiac spheroids with SB 431542, a selective inhibitor of TGF-b type I receptor, resulted in a reduction in the size of spheroids, which was accompanied by a decrease in parasite load and in fibronectin expression.
TGFBR1/2 genetic variants (in particular when evaluated as a burden by score) might play a role in modulating the severity of cardiovascular manifestation in Marfan syndrome.
Inhibition of each TGFbeta receptor-I, glucocorticoid receptor or JNK signaling partially reversed the dexamethasone-mediated effects, suggesting a complex signaling network. These data reveal that dexamethasone mediates progression by membrane effects and binding to glucocorticoid receptor
DZNep induced miR-202-5p to target both TGFbeta receptors, TGFBR1 and TGFBR2...transfection of anti-miRNAs against miR-202-5p resulted in increased TGFBR1 and TGFBR2 protein expressions and induced EMT characteristics in these cells. In stellate pancreatic cells, miR-202 overexpression slowed growth as well as reduced stromal extracellular membrane matrix protein expression
Findings provide evidence that TGFBR-1 expression is regulated by SLC35F2 which exerts its oncogenic effect on papillary thyroid carcinoma progression through activation of TGFBR-1 and ASK-1.
rs334348 polymorphism may influence individual's susceptibility to endometriosis and its severity
miR-130a-3p might play a critical role in negatively regulating hepatic stellate cell activation and proliferation in the progression of nonalcoholic fibrosing steatohepatitis by directly targeting TGFBR1 and TGFBR2 via the TGF-beta/SMAD signaling pathway.
TGFbetaR1 signaling was involved in 14-3-3zeta-mediated cell proliferation and metastasis of lung squamous cell carcinoma cells.
Mutational activation of BRAF confers sensitivity to TGFBR1 inhibitors in human melanoma cells.
Loeys-Dietz syndrome patients with confirmed mutations in TGFBR1 or TGFBR2 had an increased prevalence of inflammatory bowel disease
ALK5 is an important mediator of HTFs fibrosis. ALK5 is a potential therapeutic target to suppress scar formation after filtration surgery.
PAR2 is crucial for TGF-beta1-induced cell motility by its ability to sustain expression of ALK5. Therapeutically targeting PAR2 may thus be a promising approach in preventing TGF-beta-dependent driven metastatic dissemination in PDAC and possibly other stroma-rich tumour types.
results suggest a role for prostatic expression of TGF-B, IL-1a, TGFBRI and TGFBRII as prognostic markers for prostate cancer. The rational combination of novel agents directed toward the inactivation of TGF-B, IL-1a, TGFBRI and TGFBRII could disrupt complementary tumor cell proliferation pathways.
Data show that twist-related protein 1 (Twist1) requires TGF-beta type-I receptor (TGFBR1)-activation for activation for epithelial-mesenchymal transition (EMT)-induction.
This study shows that TFAP2C promoted lung tumor progression by upregulation of TGFBR1 and consequent activation of PAK1 signaling.
combined inhibition of ALK5 and CTGF is required to prevent TGFbeta-induced nodule formation in tri-cellular cultures
Aortic diseases in patients with TGFBR1 or TGFBR2 mutations show the same prevalence of systemic features and the same global survival.
In this small cohort, the results did not reach significance to identify the TFGBR1*6A allele as a major modifier for aortic dilation, ectopia lentis, or systemic features associated with MFS or other connective tissue disorders.
miR-181a promoted porcine preadipocyte differentiation by directly targeting TGFBR1.
The results indicate that the TGFBR1 gene polymorphism (SNP64) is significantly associated with growth rates including average daily gains between birth and 56 kg, between 5.5 and 56 kg, between 35 and 56 kg.
Report temporal regulation of TGFBR1 mRNA expression in the oocyte, granulosa and theca cells of developing preovulatory follicles in the pig.
TGFbeta is abundant in boar seminal plasma, thus TGFbeta may be a male-female signalling agent involved in immune changes in the female reproductive tract elicited by seminal fluid.
Porcine transforming growth factor beta receptor 1 has many polymorphisms, including two nonsynonymous substitutions in exons 1 and 7 and novel alternative splicing in exon 3.
isolation and molecular characterization; the full-length TGFBR1 cDNA 1813 bp contains an open reading frame (ORF) of 1512 bp encoding a TGFBR1 protein of 503 amino acids with a calculated molecular weight of 56.4 kDa.
found in binucleate cells of placenta
Results show that ALK5 and ALK1 play antagonistic roles in TGF-beta-induced podosome formation in aortic endothelial cells.
This study showed that ubiquitinated ALK5 and phosphorylated heat shock protein 27 specifically accumulate in the cytoskeleton fraction, and ALK1 and ALK5 interact with heat shock protein 90.
GM-CSF induced airway smooth muscle cells to increase expression of transforming growth factor (TGF)-beta receptors type I, II, and III, but had no detectable effect on the release of TGF-beta1 by the same ASMC; corticosteroids were inhibitory
ALK5 and Smad4 have roles in TGF-beta1-induced pulmonary endothelial permeability
These results indicate that high plasma cholesterol levels may contribute to the pathogenesis of certain diseases (e.g., atherosclerosis) by suppressing TGF-beta responsiveness.
Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5.
ALK1 and ALK5 are both essential for correct regulation of VEGF, and that disruption of either pathway leads to disease.
TGF-beta1 downregulates caveolin-1 of cultured endothelial cells, involving ALK-5 receptor subtype
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.
TGF-beta receptor type I
, TGF-beta receptor type-1
, TGF-beta type I receptor
, activin A receptor type II-like kinase, 53kD
, activin A receptor type II-like kinase, 53kDa
, activin A receptor type II-like protein kinase of 53kD
, activin receptor-like kinase 5
, serine/threonine-protein kinase receptor R4
, transforming growth factor beta receptor I
, transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kD)
, transforming growth factor-beta receptor type I
, transforming growth factor, beta receptor 1 (activin A receptor type II-like kinase, 53kDa)
, transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kDa)
, transforming growth factor beta type I receptor
, transforming growth factor, beta receptor 1
, transforming growth factor beta receptor 1
, activin A receptor type II-like kinase
, transforming growth factor beta receptor type I
, transforming growth factor beta, receptor 1
, type I serine/threonine kinase receptor
, TGF-beta receptor type-1-like
, transforming growth factor, beta receptor I
, transforming growth factor, beta receptor 1 a
, transforming growth factor, beta receptor I a
, transforming growth factor-beta receptor type I a