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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
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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 (zeige TGFB1 Proteine) on cell proliferation and induction of invasive metastatic behavior
data implies that miR (zeige MLXIP Proteine)-140 is a potent chondrogenic differentiation inducer for iPSCs and also, we have showed increasing chondrogenic differentiation by using overexpression of miR (zeige MLXIP Proteine)-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 (zeige TGFB1 Proteine) and TGFb3, but not TGFb2 (zeige TGFB2 Proteine), 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 (zeige TGFB1 Proteine)) 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 (zeige MLXIP Proteine)-494 in decidual mesenchymal stem cells (MSC (zeige MSC Proteine)) and attenuates the regulation of MSC (zeige MSC Proteine) 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 (zeige CPOX Proteine)).
combining TGF-beta3 with BMP-2 (zeige BMP2 Proteine) was able to promote the process of bone formation more markedly in vitro, providing a promising clinical strategy in the field of skeletal regeneration and in fracture healing.
No significant association was observed in MMP13 (zeige MMP13 Proteine), TIMP2 (zeige TIMP2 Proteine) and TGFB3 genes with CP or PI. CP is a risk factor to develop PI, however, there is no association of both diseases with polymorphisms in the MMP13 (zeige MMP13 Proteine), TIMP2 (zeige TIMP2 Proteine) and TGFB3 genes
Results suggest that the miR (zeige MLXIP Proteine)-140-3p is involved in osteoblast differentiation as a critical regulatory factor between Wnt3a (zeige WNT3A Proteine) and TGFbeta3 signaling pathways.
Egr2 (zeige EGR2 Proteine) and Egr3 (zeige EGR3 Proteine) 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 (zeige CFB Proteine) (TGF-b) and mitogen activated protein kinase (zeige MAPK1 Proteine) (MAPK (zeige MAPK1 Proteine)) signalling pathways in cardiac fibrosis
Data (including data from studies using knockout mice) suggest Garp/Lrrc32 (zeige LRRC32 Proteine) is involved in up-regulation of Tgfb3 and is essential for normal embryogenesis of palate; knockout of Garp (zeige LRRC32 Proteine) causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 (zeige SMAD2 Proteine) phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Garp (zeige LRRC32 Proteine) = glycoprotein A repetitions predominant (zeige LRRC32 Proteine) protein; Smad2 (zeige SMAD2 Proteine) = MAD homolog protein 2)
TGFb3-induced down-regulation of p63 (zeige CKAP4 Proteine) 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 (zeige TGFB1 Proteine) and TGF-beta3 existed in ConA-induced acute autoimmune liver injury.
CCN4 (zeige WISP1 Proteine) 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.
TGF-beta3-expressing CD4 (zeige CD4 Proteine)+CD25 (zeige IL2RA Proteine)(-)LAG3 (zeige LAG3 Proteine)+ regulatory T cells have a role in controlling humoral immune responses
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 (zeige TNMD Proteine) and Thrombospondin-4 (zeige THBS4 Proteine).
TGFbeta (zeige TGFB1 Proteine) 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 (zeige TGFB1 Proteine)) is required for hematopoietic progenitor cell specification. The requirement for TGFbeta (zeige TGFB1 Proteine) 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 (zeige PTPN14 Proteine) plays a crucial role in organogenesis by inducing TGFbeta (zeige TGFB1 Proteine) 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