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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
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)).
combining TGF-beta3 with BMP-2 (show BMP2 Proteins) 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 (show MMP13 Proteins), TIMP2 (show TIMP2 Proteins) 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 (show MMP13 Proteins), TIMP2 (show TIMP2 Proteins) and TGFB3 genes
Our study showed that TGFA (show TGFA Proteins)/TGFB3/MSX1 (show MSX1 Proteins) gene polymorphisms were associated with congenital NSHI. CCGTAC and TTACGT haplotypes might be protective factors, while TTGCGC haplotype might be a risk factor for congenital NSHI. TGFA (show TGFA Proteins)/TGFB3/MSX1 (show MSX1 Proteins) gene rs3771494, rs1058213, rs3917201, rs2268626, rs3821949, and rs62636562 haplotype analysis showed that haplotype CCGTAC and TTACGT might be protective factors (both P<0.001)
increased stromal POSTN (show POSTN Proteins) induced by TGF-beta3 directly accelerated the growth, migration and invasion of cancer cells
Taken together, these results demonstrate that insulin (show INS Proteins) and TGF-beta3 present antagonistic effects during the chondrogenesis of human bone marrow-derived stem/progenitor cells.
CCN4 (show WISP1 Proteins) has a positive influence on chondrogenic differentiation by modulating the effects of TGF-beta3.
TGFB3 polymorphism is associated with male infertility.
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.
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 (show CD4 Proteins)+CD25 (show IL2RA Proteins)(-)LAG3 (show LAG3 Proteins)+ regulatory T cells have a role in controlling humoral immune responses
Pathological TGF-beta (show TGFB1 Proteins) release from osteolytic bone metastases contributes to muscle weakness in cancer by decreasing Ca(2 (show CA2 Proteins)+)-induced muscle force production.
Ephrin reverse signaling mediates palatal fusion and epithelial-to-mesenchymal transition independently of Tgfss3.
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