Browse our TGFBR1 Proteins (TGFBR1)

Human Transforming Growth Factor, beta Receptor 1 (TGFBR1) interaction partners

1. reduction or deletion of TbetaR2 or NF2 induces the TbetaR1-mediated oncogenic pathway, and therefore inhibition of the unbalanced TGFbeta signaling is a putative strategy for NF2-related cancers

2. Data indicate that PPAR-g agonists represent an attractive treatment tool and by suppression of cell growth (in vitro and ex vivo models) and of invasion via blockade of MAPK cascade and TGFb/SMADs signaling, respectively, and its role in cancer bioenergetics and metabolism indicate that PPAR-g agonists represent an attractive treatment tool for non small cell lung cancer .

3. interferon consensus sequence-binding protein upregulates transforming growth factor-beta type I receptor (TGF-beta RI) expression by binding to nucleotides -216/-211 (GGXXTC) in the TGF-beta RI promoter, which resulted in increased tumorigenicity and tumor progression in human osteosarcoma cells.

4. Study showed that TNFRSF19 is highly expressed in nasopharyngeal carcinoma (NPC) and is required for cell proliferation and NPC development. TNFRSF19 was not involved in NFkappaB activation or associated with TRAF proteins. TbetaRI was identified as a specific binding partner for TNFRSF19. TNFRSF19 bound the kinase domain of TbetaRI in the cytoplasm, thereby blocking Smad2/3 association with TbetaRI and subsequent sign...

5. loss of the co-expression of PRLR, TGFbetaRI and TGFbetaRII is indicative of aggressiveness and poor patient survival outcomes in breast cancer.

6. Downregulation of CYLD promotes invasion with mesenchymal transition via ALK5 stabilization in oral squamous cell carcinoma cells.

7. AHNAK interference restored the hepatocellular carcinoma (HCC) cell invasion and metastasis deprived by RNF38 downregulation. Clinically, elevated RNF38 and transforming growth factor beta receptor 1 (TGFBR1) expression was related to short overall survival (OS) and high cumulative recurrence rates in HCC patients.

8. Experimental results indicate that HA can antagonize TGF-beta1 effect on EMT and mucociliary differentiation of NECs by down-regulation of TbetaR I, which is via CD44.

9. First evidence of maternally inherited mosaicism in TGFBR1 and subtle primary myocardial changes in Loeys-Dietz syndrome has been reported. (Case reports)

10. hese studies indicate that TGFbeta signaling through TGFBR1/ALK5 in the endometrium is required for endometrial homeostasis, tumor suppression, and postpartum endometrial regeneration.

11. TGFBR1 mutations were more frequent among Loeys-Dietz syndrome patients with motor delays and feeding issues.

12. Results show that TGFBR1 is upregulated in nonsmall cell lung cancer (NSCLC) that its 3'UTR is a direct target for miR98.

13. Mutations in TGFBR1 exon 5 cause either Loeys-Dietz syndrome or multiple self-healing squamous epithelioma.

14. The majority of the identified P/LP variants were in the FBN1 gene ..we found 4.9% of patients carried a P/LP variant as the underlying cause of their Thoracic aortic aneurysm/aortic dissection (TAAD), predominantly within FBN1 but with substantial contributions from TGFBR and COL genes.

15. Long non-coding RNA SBF2-AS1 modulated TGFBR1 through sponging miR-140-5p in hepatocellular carcinoma development and progression.

16. GPR50 is a TbetaRI co-receptor with potential impact on cancer development

17. Systemic activation of Activin A signaling causes chronic kidney disease-mineral bone disorder. (Review)

18. TGFbetaR1 rs10739778 was associated with blood pressure in healthy pregnant women.

19. 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.

20. 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.

Pig (Porcine) Transforming Growth Factor, beta Receptor 1 (TGFBR1) interaction partners

1. miR-181a promoted porcine preadipocyte differentiation by directly targeting TGFBR1.

2. 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.

3. Report temporal regulation of TGFBR1 mRNA expression in the oocyte, granulosa and theca cells of developing preovulatory follicles in the pig.

4. 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.

5. 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.

6. 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.

Cow (Bovine) Transforming Growth Factor, beta Receptor 1 (TGFBR1) interaction partners

1. found in binucleate cells of placenta

2. Results show that ALK5 and ALK1 play antagonistic roles in TGF-beta-induced podosome formation in aortic endothelial cells.

3. 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.

4. 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

5. ALK5 and Smad4 have roles in TGF-beta1-induced pulmonary endothelial permeability

6. These results indicate that high plasma cholesterol levels may contribute to the pathogenesis of certain diseases (e.g., atherosclerosis) by suppressing TGF-beta responsiveness.

7. Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5.

8. ALK1 and ALK5 are both essential for correct regulation of VEGF, and that disruption of either pathway leads to disease.

9. TGF-beta1 downregulates caveolin-1 of cultured endothelial cells, involving ALK-5 receptor subtype

Mouse (Murine) Transforming Growth Factor, beta Receptor 1 (TGFBR1) interaction partners

1. This study provides a novel mouse model of testicular granulosa cell tumors and uncovered tumorigenic function of enhanced TGFB signaling in the testis.

2. The biologic effects of two transforming growth factor beta receptor 1 (TGFBR1) kinase inhibitors designed to target TGFbeta signaling.

3. hese studies indicate that TGFbeta signaling through TGFBR1/ALK5 in the endometrium is required for endometrial homeostasis, tumor suppression, and postpartum endometrial regeneration.

4. GPR50 is a TbetaRI co-receptor with potential impact on cancer development

5. TGFBR1 is a target gene of miR-22 during C2C12 myoblast differentiation.

6. Postnatal cartilage-specific deletion of Alk5 induced an OA-like phenotype with degradation of articular cartilage, synovial hyperplasia, osteophyte formation, subchondral sclerosis, as well as enhanced chondrocyte apoptosis, overproduction of catabolic factors, and decreased expressions of anabolic factors in chondrocytes. In addition, the expressions of PRG4 mRNA and protein were decreased in Alk5 conditional KO mice.

7. Loss of ALK5 is associated with germinal matrix hemorrhage-intraventricular hemorrhage.

8. this study shows that tissue-specific differentiation of colonic macrophages requires TGFbeta receptor-mediated signaling

9. Taken together, these results indicate that eIF6 may be involved in external mechanical force-mediated murine dermal fibroblast function at least partly through the TGF-beta1/TGFBR1/TGFBR2 pathway.

10. expression induced by IL-6 in keratinocytes

11. Loss of smooth muscle cell-Tgfbr1 triggers multiple deleterious pathways, including abnormal TGFBR2, ERK, and AngII/AT1R signals that disrupt aortic wall homeostasis to cause aortic aneurysm formation

12. 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.

13. Deletion of smooth muscle cell-specific Tgfbr1 inhibits arterial neointimal hyperplasia in short term, but promotes an undesired vascular phenotype for injured arteries.

14. TGFbetaR1 signalling is needed for development of CD103(+)CD11b(+) intestinal DCs from CD103(-)CD11b(+) cells and that they contribute to the generation of Th17 and regulatory T cells.

15. Overactivation of TGFBR1 drives gonadal tumor development. The TGFBR1 constitutively active mouse model phenocopies a number of morphological, hormonal, and molecular features of human granulosa cell tumors and are potentially valuable for preclinical testing of targeted therapies to treat granulosa cell tumors, a class of poorly defined ovarian malignancies.

16. results indicate that CD34+ cells and signaling through ALK5 play pivotal roles in the morphogenesis of interstitial-like, peritubular-like and cord-like structures

17. a novel role for SREBP-1 as a cell surface retention factor for TbetaRI in mesangial cells, is reported.

18. a surface population of Hsp90 extracellularly binds TGFbetaRI and this complex behaves as an active participant in collagen production in TGFbeta-activated fibroblasts.

19. Conditional deletion of Tgfbr1 in PTEN-inactivated endometrium leads to a disease that recapitulates invasive and lethal human endometrial cancer.

20. fluid shear stress induces autocrine TGF-beta/ALK5-induced target gene expression in renal epithelial cells, which is partially restrained by MEK1/2-mediated signaling.