Transforming Growth Factor, beta Receptor III (TGFBR3) ELISA Kits

Cow (Bovine) Transforming Growth Factor, beta Receptor III (TGFBR3) interaction partners

1. Inhibition of genes for betaglycan and FIBP in granulosa cells in vitro suggests that they inhibit estradiol production in regressing subordinate follicles.

Human Transforming Growth Factor, beta Receptor III (TGFBR3) interaction partners

1. We suggest that TGFBR3 protein expression is involved in up-regulated TGF-beta signaling in Marfan syndrome patients with a dominant negative FBN1 gene mutation.

2. describe a detailed characterization of TbetaRIII expression in lymphocyte subpopulations demonstrating that this co-receptor is significantly expressed in T but not B lymphocytes and among them, preferentially expressed on naive and central memory T cells

3. TGF-beta type I, II, and III receptors were all identified in pregnant serum; all were substantially elevated in early-onset but not late-onset PE. Endoglin was increased in both subtypes.

4. TGFBR3 and/or MGEA5 rearrangements are much more common in hybrid hemosiderotic fibrolipomatous tumor-myxoinflammatory fibroblastic sarcomas than in classical myxoinflammatory fibroblastic sarcomas.

5. opposing functions for the different GAG modifications on TbetaRIII suggesting that Wnt interactions with the TbetaRIII heparan sulfate chains result in inhibition of Wnt signaling, likely via Wnt sequestration, whereas the chondroitin sulfate GAG chains on TbetaRIII promote Wnt3a signaling.

6. Results suggest that high expression levels of alpha-inhibin and beta-glycan transcripts in secretory phase endometrium are associated with a lower chance of achieving pregnancy with in vitro fertilization.

7. Results show decreased TbetaRIII expression with hepatocellullar carcinoma (HCC) progression leading to the activation of Smad2 and suggest that TbetaRIII acts as a suppressive factor in regulating the migration and invasion of HCC, by inhibiting Smad2 and Akt pathways.

8. Study shows that TbetaRIII expression is significantly decreased in salivary glands adenoid cystic carcinoma (ACC) patients and defines TbetaRIII as a biomarker exerting antitumor action on ACC progression.

9. No correlation of loss of heterozygosity at the TGFBR3 locus with clinicopathological parameters suggests that allelic imbalance may be an early genetic event during neoplastic transformation of human endometrium.

10. Study shows that GDF10 is down-regulated in patients with oral squamous cell carcinoma, and is an independent risk factor for overall survival. Its expression is regulated by TGFBR3 which shares the signaling inhibiting epithelial-mesenchymal transition.

11. Data suggest a high potential of plasma sTBFbetarIII as a novel diagnostic and prognostic biomarker in breast cancer.

12. rs1192415 of TGFBR3 is associated with primary open angle glaucoma.

13. results suggest overexpression of TbetaRIII receptor restored TGF-beta1 sensitivity in CAL-27 cells

14. The presence of the index SNP rs1192415 (TGFBR3-CDC7) was associated with visual field progression in POAG (primary open-angle glaucoma) patients.

15. Inhibiting ectodomain shedding of TbetaRIII increased TGF-beta responsiveness and abrogated TbetaRIII's ability to inhibit breast cancer cell migration and invasion.

16. RS1805110 is not associated with Behcet's disease or idiopathic intermediate uveitis in Caucasian patients.

17. data suggest complex or phenotype specific association of cryptorchidism with TGFBR3 and the gubernaculum as a potential target of TGFbeta signaling

18. We have found that TbetaRIII is required for migration and invasion in vitro and xenograft growth in vivo.

19. Data indicate that TGF-beta2 (TGFB2) and TGF beta type III receptor (TGFBR3) are target genes of miR-193b in chondrogenesis.

20. These data demonstrate that TbetaRIII regulates BMP-mediated signaling and biological effects, primarily through the ligand sequestration effects of sTbetaRIII in normal and cancerous mammary epithelial cells.

Mouse (Murine) Transforming Growth Factor, beta Receptor III (TGFBR3) interaction partners

1. TGFbetaR3 promotes apoptosis of cardiomyocytes via a p38 pathway-associated mechanism, and loss of TGFbetaR3 reduces myocardial infarction injury.

2. BMP2 also requires Src for filamentous actin polymerization in Tgfbr3(-/-) epicardial cells.

3. describe a detailed characterization of TbetaRIII expression in lymphocyte subpopulations demonstrating that this co-receptor is significantly expressed in T but not B lymphocytes and among them, preferentially expressed on naive and central memory T cells

4. Study identified a novel major binding site for TGF-beta-like growth factors in TGFR-3. Findings potentially provide novel experimental insight into the general function of zona pellucida domain-containing proteins.

5. a signaling pathway important in epicardial cell behavior downstream of TGFbetaR3

6. Retinoic acid enhanced TbetaRIII expression and that this increase contributed to LF-stimulated IgA production.

7. Pro-fibrotic cardiac effect of miR-328 was mediated by down-regulating TGFbR3 and up-regulating TGFb1.

8. These data reveal a critical, previously unrecognized role for TGFbetaR3 in vascular and osteoblast development during palatogenesis.

9. These data demonstrate that TbetaRIII regulates BMP-mediated signaling and biological effects, primarily through the ligand sequestration effects of sTbetaRIII in normal and cancerous mammary epithelial cells.

10. Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-beta signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts.

11. work reveals a 'seed and soil' mechanism where TGF-beta2 and TGF-beta-RIII signalling through p38alpha/beta regulates DTC dormancy and defines restrictive (BM) and permissive (lung) microenvironments for HNSCC metastasis

12. TGFBR3 mediated suppression of cancer progression includes effects on the tumor immune microenvironment.

13. Loss of Tgfbr3 compromises the functions of TGFbeta2 in the differentiating fetal testis.

14. A novel reciprocal loop between miR-21 and TGFbetaRIII in cardiac fibrosis caused by myocardial infarction in mice.

15. These data suggest that Inhibins and TbetaRIII may function as a molecular pair regulating T cell development.

16. the relative roles of TGFbetaR3-dependent and -independent signaling in the actions of BMP2 on epicardial cell behavior and demonstrate the critical role of TGFbetaR3 in mediating BMP2-stimulated invasion.

17. used intact embryos and epicardial cells from E11.5 mouse embryos to reveal the mechanisms by which TGFbetaR3 signals and regulates epicardial cell behavior

18. TGFBR3 can prevent hypoxia-induced injury in neonatal mice cardiac fibroblasts by negative regulation of TGF-beta signaling.

19. Data present the 2.0-A resolution crystal structure of the betaglycan ZP-C region in combination with a downstream region known as the external hydrophobic patch.

20. The expressions of TGF-beta3 and TbetaR-III in MEE were temporally correlated with critical events in palatogenesis.

Pig (Porcine) Transforming Growth Factor, beta Receptor III (TGFBR3) interaction partners

1. This study provides evidence that the expressions of inhibin alpha subunit and betaglycan are inferior in cystic follicles, and this may be caused by the decrease in FSH in the presence of a cystic follicle.