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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
YOD1 RNAi may inhibit cell proliferation and migration associated with the pathogenesis of NSCL/P through TGF-beta3 signaling. The study indicates a novel role of YOD1 in regulating TGF-beta3 signaling to affect cell proliferation and migration resulting in cleft lip with or without cleft palate.
Elevations of TGF-beta3, SMAD2 and SMAD4 in hypertrophic scars and increase of IGF-1R in immature stages may give some clues for acne hypertrophic scar formation.
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 isoforms.
This study showed that YOD1 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 on cell proliferation and induction of invasive metastatic behavior
data implies that miR-140 is a potent chondrogenic differentiation inducer for iPSCs and also, we have showed increasing chondrogenic differentiation by using overexpression of miR-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 and TGFb3, but not TGFb2, showed higher expression levels in invasive breast cancer compared to normal tissues.
In nonsyndromic CL+/-P Malay patients,the prevalence of the mutations in the TGFbeta3 gene was 17.7%. For the TGFbeta3 gene, there was no mutation in the coding region in either of the groups.
Cancer cachexia promotes the development of adipose tissue (AT) fibrosis, in association with altered transforming growth factor-beta (TGFbeta) signaling, compromising AT organization and function.
Human dental apical papilla-derived Mesenchymal stem cells (hSCAPs) can produce and secrete TGFbeta3 in response to micro-environmental cues.
Higher TGF-beta3 serum concentrations are a risk factor for uterine fibroids.
High expression of TGF-beta3 in preeclampsia decidua stimulates miR-494 in decidual mesenchymal stem cells (MSC) and attenuates the regulation of MSC 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).
combining TGF-beta3 with BMP-2 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, TIMP2 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, TIMP2 and TGFB3 genes
Our study showed that TGFA/TGFB3/MSX1 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/TGFB3/MSX1 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 induced by TGF-beta3 directly accelerated the growth, migration and invasion of cancer cells
Taken together, these results demonstrate that insulin and TGF-beta3 present antagonistic effects during the chondrogenesis of human bone marrow-derived stem/progenitor cells.
CCN4 has a positive influence on chondrogenic differentiation by modulating the effects of TGF-beta3.
The comparison of transforming growth factor beta family (TGFbeta) expression showed significantly higher levels of Tgfbeta3 transcript between nude and Balb/c mice but no differences were detected for Tgfbeta1. Nude DFs were specifically sensitive to the presence of the pro-regenerative TGFbeta3 isoform, showing increased collagen I deposition and alpha smooth muscle actin expression.
Data indicated that autophagy was required for TGF-beta3 induced airway mucous hyper-production.
Results suggest that the miR-140-3p is involved in osteoblast differentiation as a critical regulatory factor between Wnt3a and TGFbeta3 signaling pathways.
Egr2 and Egr3 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 (TGF-b) and mitogen activated protein kinase (MAPK) signalling pathways in cardiac fibrosis
Data (including data from studies using knockout mice) suggest Garp/Lrrc32 is involved in up-regulation of Tgfb3 and is essential for normal embryogenesis of palate; knockout of Garp causes postnatal lethality, cleft palate, and decreased apoptosis and Smad2 phosphorylation in medial edge epithelial cells of palatal shelf of embryos. (Garp = glycoprotein A repetitions predominant protein; Smad2 = MAD homolog protein 2)
TGFb3-induced down-regulation of p63 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 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+CD25(-)LAG3+ regulatory T cells have a role in controlling humoral immune responses
Pathological TGF-beta release from osteolytic bone metastases contributes to muscle weakness in cancer by decreasing Ca(2+)-induced muscle force production.
Ephrin reverse signaling mediates palatal fusion and epithelial-to-mesenchymal transition independently of Tgfss3.
TGF-beta3 significantly downregulates JAM-B expression via post-transcriptional and post-translational modulation and results in the disruption of BTB and apical ES.
Controlled chondrogenesis from adipose-derived stem cells by recombinant transforming growth factor-beta3 fusion protein in peptide scaffolds.
TGF-beta3 mediates palate fusion in part by down-regulating Jagged2 expression in palatal medial edge epithelium.
periderm degeneration depends on functional TGFbeta3 signaling to repress DeltaNp63, thereby coordinating periderm desquamation
This study provides a comprehensive list of genes differentially expressed in the healing corneal epithelial cells of diabetic corneas and suggests the therapeutic potential of TGF-beta3 for treating corneal and skin wounds in diabetic patients.
Transforming growth factor-beta3 (TGF-beta3) knock-in ameliorates inflammation due to TGF-beta1 deficiency while promoting glucose tolerance.
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 and Thrombospondin-4.
TGFbeta 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) is required for hematopoietic progenitor cell specification. The requirement for TGFbeta 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...
Proper cranial neural crest formation and survival, and ultimately craniofacial chondrogenesis and osteogenesis, are dependent on tight regulation of Tgfbeta3 protein levels in zebrafish.
These data suggest Pez plays a crucial role in organogenesis by inducing TGFbeta 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.
The mTGF-beta3 fusion protein was successfully expressed after transfection.
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