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Human TGFB3 Protein expressed in Tobacco (Nicotiana benthamiana) - ABIN1112031
ten Dijke, Hansen, Iwata, Pieler, Foulkes: Identification of another member of the transforming growth factor type beta gene family. in Proceedings of the National Academy of Sciences of the United States of America 1988
Show all 4 Pubmed References
This review highlights advances in the understanding of the cellular sources, activation processes, contextual determinants, and immunological roles of TGF-beta3 with comparisons to other TGF-beta (show TGFB1 Proteins) isoforms.
This study showed that YOD1 (show YOD1 Proteins) overexpression enhances cell migration by promoting TGF-beta3 signaling which may play an important role in lip and palate formation.
We suggest that increased TGFbeta3 levels are responsible for development of aggressive prostate cancer in African American patients as a consequence of development of resistance to inhibitory effects of TGFbeta (show TGFB1 Proteins) on cell proliferation and induction of invasive metastatic behavior
data implies that miR (show MLXIP Proteins)-140 is a potent chondrogenic differentiation inducer for iPSCs and also, we have showed increasing chondrogenic differentiation by using overexpression of miR (show MLXIP Proteins)-140 and TGFbeta3.
The increase in TGF-beta3 found in inflammatory wound healing (WF) highlights its negative effect on wound healing, while the increased levels of sEng in granulating WF affects the leukocyte adhesion/transmigration through the endothelium, reducing the inflammatory response and favoring the wound healing.
Data indicate that TGFb1 (show TGFB1 Proteins) and TGFb3, but not TGFb2 (show TGFB2 Proteins), showed higher expression levels in invasive breast cancer compared to normal tissues.
Cancer cachexia promotes the development of adipose tissue (AT) fibrosis, in association with altered transforming growth factor-beta (TGFbeta (show TGFB1 Proteins)) signaling, compromising AT organization and function.
Higher TGF-beta3 serum concentrations are a risk factor for uterine fibroids.
High expression of TGF-beta3 in preeclampsia decidua stimulates miR (show MLXIP Proteins)-494 in decidual mesenchymal stem cells (MSC (show MSC Proteins)) and attenuates the regulation of MSC (show MSC Proteins) switching the macrophage toward M2 type, contributing to an immune imbalance at maternal-fetal interface.
The frequency GA genotype of transforming growth factor beta 3 (TGFbeta3) gene was associated with increased risk of non-syndromic cleft palate only (NS CPO (show CPOX Proteins)).
Data indicated that autophagy was required for TGF-beta3 induced airway mucous hyper-production.
Results suggest that the miR (show MLXIP Proteins)-140-3p is involved in osteoblast differentiation as a critical regulatory factor between Wnt3a (show WNT3A Proteins) and TGFbeta3 signaling pathways.
Egr2 (show EGR2 Proteins) and Egr3 (show EGR3 Proteins) expressed in T cells cooperatively prevent humoral immune responses by supporting TGF-beta3 secretion.
We identified TGF-beta3 as the top-ranked gene, a critical component of the transforming growth factor-b (show CFB Proteins) (TGF-b) and mitogen activated protein kinase (show MAPK1 Proteins) (MAPK (show MAPK1 Proteins)) signalling pathways in cardiac fibrosis
Data (including data from studies using knockout mice) suggest Garp/Lrrc32 (show LRRC32 Proteins) is involved in up-regulation of Tgfb3 and is essential for normal embryogenesis of palate; knockout of Garp (show LRRC32 Proteins) causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 (show SMAD2 Proteins) phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Garp (show LRRC32 Proteins) = glycoprotein A repetitions predominant (show LRRC32 Proteins) protein; Smad2 (show SMAD2 Proteins) = MAD homolog protein 2)
TGFb3-induced down-regulation of p63 (show CKAP4 Proteins) in the medial edge epithelia of the palatal shelves is a pre-requisite for palatal fusion by facilitating periderm migration from, and reducing the proliferative potential of, the midline epithelial seam thereby preventing cleft palate.
Early activation of hepatic stellate cell and imbalance expression of TGF-beta1 (show TGFB1 Proteins) and TGF-beta3 existed in ConA-induced acute autoimmune liver injury.
CCN4 (show WISP1 Proteins) has a positive influence on chondrogenic differentiation by modulating the effects of TGF-beta3.
TGFbeta3 increases IRF6 expression and subsequently regulates SNAI2 expression; IRF6 appears to regulate epithelial mesenchymal transition during palatal fusion via SNAI2.
Analysis of the Tgf-beta-3 knockout mouse model has enabled identification of miRNAs with altered expression that may contribute to the cleft palate phenotype.
The addition of TGF-beta3 to the 3D cultures further up-regulates the expression of these genes and also induces the expression of mature tenocyte markers Tenomodulin (show TNMD Proteins) and Thrombospondin-4 (show THBS4 Proteins).
TGFbeta (show TGFB1 Proteins) may play a role in the overall process of luteinization, but it appears not to influence steroidogenesis in luteinizing pig follicles.
In swine, TGF-beta3 mRNA is expressed throughout the oestrus cycle.
transforming growth factor beta (TGFbeta (show TGFB1 Proteins)) is required for hematopoietic progenitor cell specification. The requirement for TGFbeta (show TGFB1 Proteins) is two fold and sequential: autocrine via Tgfbeta1a and Tgfbeta1b produced in the endothelial cells themselves, followed by a paracrine input of Tgfbeta3 from the notochord, suggesting that the former programs the hemogenic endothelium and the latter drives endothelial-to-hematopoietic tran...
These data suggest Pez (show PTPN14 Proteins) plays a crucial role in organogenesis by inducing TGFbeta (show TGFB1 Proteins) and epithelial-mesenchymal transition.
Tissues exposed to TGF-beta3 had significantly increased glycosaminoglycan and total collagen protein production along with upregulated cartilage-specific gene expression, resulting in tissues with a higher Young's Modulus
Data show that TGF-beta pathways operate during ovarian fetal development, and fibrillin 3 is highly expressed at a critical stage early in developing human and bovine fetal ovaries.
This gene encodes a member of the TGF-beta family of proteins. The encoded protein is secreted and is involved in embryogenesis and cell differentiation. Defects in this gene are a cause of familial arrhythmogenic right ventricular dysplasia 1.
transforming growth factor, beta 3
, transforming growth factor beta-3
, transforming growth factor beta-3 preproprotein
, transforming growth factor beta-3-like
, transforming growth factor-beta3
, transforming growth factor b3
, transforming growth factor-beta 3
, protein kinase
, tgf beta 3