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抗Human TGFBR1 抗体:
抗Mouse (Murine) TGFBR1 抗体:
抗Rat (Rattus) TGFBR1 抗体:
Human Polyclonal TGFBR1 Primary Antibody for IF (p), IHC (p) - ABIN671256
Xie, Chen, Miao, Tang, Fu: Regulation of cellular behaviors of fibroblasts related to wound healing by sol-gel derived bioactive glass particles. in Journal of biomedical materials research. Part A 2016
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Human Polyclonal TGFBR1 Primary Antibody for IHC (p), WB - ABIN392279
Miles, Tung, Aguiar, Kurtoglu, Sikes: Increased TGF-?1-mediated suppression of growth and motility in castrate-resistant prostate cancer cells is consistent with Smad2/3 signaling. in The Prostate 2012
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Human Polyclonal TGFBR1 Primary Antibody for IF, WB - ABIN317892
Yu, Hu, Yang, Takemori, Li, Zheng, Hong, Liao, Wen: Salt-inducible kinase 1 is involved in high glucose-induced mesangial cell proliferation mediated by the ALK5 signaling pathway. in International journal of molecular medicine 2013
Human Polyclonal TGFBR1 Primary Antibody for ELISA, WB - ABIN563176
Matsunobu, Torigoe, Ishikawa, de Vega, Kulkarni, Iwamoto, Yamada: Critical roles of the TGF-beta type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate development. in Developmental biology 2009
Mouse (Murine) Monoclonal TGFBR1 Primary Antibody for FACS - ABIN4896300
Bodogai, Moritoh, Lee-Chang, Hollander, Sherman-Baust, Wersto, Araki, Miyoshi, Yang, Trinchieri, Biragyn: Immunosuppressive and Prometastatic Functions of Myeloid-Derived Suppressive Cells Rely upon Education from Tumor-Associated B Cells. in Cancer research 2015
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 (显示 TGFB1 抗体) receptor-I, glucocorticoid receptor (显示 NR3C1 抗体) or JNK (显示 MAPK8 抗体) 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 (显示 NR3C1 抗体)
DZNep induced miR (显示 MLXIP 抗体)-202-5p to target both TGFbeta (显示 TGFB1 抗体) receptors, TGFBR1 and TGFBR2 (显示 TGFBR2 抗体)...transfection of anti-miRNAs against miR (显示 MLXIP 抗体)-202-5p resulted in increased TGFBR1 and TGFBR2 (显示 TGFBR2 抗体) protein expressions and induced EMT (显示 ITK 抗体) characteristics in these cells. In stellate pancreatic cells, miR (显示 MLXIP 抗体)-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 (显示 SLC35F2 抗体) which exerts its oncogenic effect on papillary thyroid carcinoma progression through activation of TGFBR-1 and ASK-1 (显示 MAP3K5 抗体).
miR (显示 MLXIP 抗体)-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 (显示 TGFBR2 抗体) via the TGF-beta (显示 TGFB1 抗体)/SMAD (显示 SMAD1 抗体) signaling pathway.
TGFbetaR1 signaling was involved in 14-3-3zeta (显示 YWHAZ 抗体)-mediated cell proliferation and metastasis of lung squamous cell carcinoma cells.
Mutational activation of BRAF (显示 BRAF 抗体) confers sensitivity to TGFBR1 inhibitors in human melanoma cells.
Loeys-Dietz syndrome patients with confirmed mutations in TGFBR1 or TGFBR2 (显示 TGFBR2 抗体) 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 (显示 F2RL1 抗体) is crucial for TGF-beta1 (显示 TGFB1 抗体)-induced cell motility by its ability to sustain expression of ALK5. Therapeutically targeting PAR2 (显示 F2RL1 抗体) may thus be a promising approach in preventing TGF-beta (显示 TGFB1 抗体)-dependent driven metastatic dissemination in PDAC and possibly other stroma-rich tumour types.
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 (显示 TGFB1 抗体) is abundant in boar seminal plasma, thus TGFbeta (显示 TGFB1 抗体) 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.
Results show that ALK5 and ALK1 (显示 ACVRL1 抗体) play antagonistic roles in TGF-beta (显示 TGFB1 抗体)-induced podosome formation in aortic endothelial cells.
This study showed that ubiquitinated ALK5 and phosphorylated heat shock protein 27 (显示 HSP27 抗体) specifically accumulate in the cytoskeleton fraction, and ALK1 (显示 ACVRL1 抗体) and ALK5 interact with heat shock protein 90 (显示 HSP90 抗体).
GM-CSF (显示 CSF2 抗体) induced airway smooth muscle cells to increase expression of transforming growth factor (TGF)-beta (显示 TGFB1 抗体) receptors type I, II, and III, but had no detectable effect on the release of TGF-beta1 (显示 TGFB1 抗体) by the same ASMC; corticosteroids were inhibitory
ALK5 and Smad4 (显示 SMAD4 抗体) have roles in TGF-beta1 (显示 TGFB1 抗体)-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 (显示 TGFB1 抗体) responsiveness.
Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5.
ALK1 (显示 ACVRL1 抗体) and ALK5 are both essential for correct regulation of VEGF (显示 VEGFA 抗体), and that disruption of either pathway leads to disease.
TGF-beta1 (显示 TGFB1 抗体) downregulates caveolin-1 (显示 CAV1 抗体) of cultured endothelial cells, involving ALK-5 receptor subtype
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.
Loss of ALK5 is associated with germinal matrix hemorrhage-intraventricular hemorrhage.
this study shows that tissue-specific differentiation of colonic macrophages requires TGFbeta (显示 TGFB1 抗体) receptor-mediated signaling
Taken together, these results indicate that eIF6 (显示 EIF6 抗体) may be involved in external mechanical force-mediated murine dermal fibroblast function at least partly through the TGF-beta1 (显示 TGFB1 抗体)/TGFBR1/TGFBR2 (显示 TGFBR2 抗体) pathway.
expression induced by IL-6 (显示 IL6 抗体) in keratinocytes
Loss of smooth muscle cell-Tgfbr1 triggers multiple deleterious pathways, including abnormal TGFBR2 (显示 TGFBR2 抗体), ERK (显示 EPHB2 抗体), and AngII/AT1R (显示 AGTRAP 抗体) signals that disrupt aortic wall homeostasis to cause aortic aneurysm formation
Deletion of smooth muscle cell-specific Tgfbr1 inhibits arterial neointimal hyperplasia in short term, but promotes an undesired vascular phenotype for injured arteries.
TGFbetaR1 signalling is needed for development of CD103 (显示 ITGAE 抗体)(+)CD11b (显示 ITGAM 抗体)(+) intestinal DCs from CD103 (显示 ITGAE 抗体)(-)CD11b (显示 ITGAM 抗体)(+) cells and that they contribute to the generation of Th17 and regulatory T cells.
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.
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