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Human Monoclonal TGFb Primary Antibody für - ABIN577154
Nishiyama, McDonough, Bruns, Burgeson: Type XII and XIV collagens mediate interactions between banded collagen fibers in vitro and may modulate extracellular matrix deformability. in The Journal of biological chemistry 1994
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Human Polyclonal TGFb Primary Antibody für IHC (p), ELISA - ABIN2476753
Goldraich, Ramos, Goldraich: Urography versus DMSA scan in children with vesicoureteric reflux. in Pediatric nephrology (Berlin, Germany) 1990
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Mouse (Murine) Monoclonal TGFb Primary Antibody für FACS, IHC - ABIN3020892
Chen, Ren, Zhang, Sun, Wang, Li, Zhang, Zhao: Disorganized vascular structures in sporadic venous malformations: a possible correlation with balancing effect between Tie2 and TGF-β. in Scientific reports 2016
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Human Monoclonal TGFb Primary Antibody für FACS, IHC - ABIN6664767
Xia, Ren, Zhu, Yu, Zhang, Sun, Zhao, Chen: Downregulation of miR-145 in venous malformations: Its association with disorganized vessels and sclerotherapy. in European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences 2017
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Cow (Bovine) Monoclonal TGFb Primary Antibody für ELISA, FACS - ABIN2476751
Mahan, Ballal, Nanda: Mitral valve tear complicating percutaneous valvuloplasty: diagnosis by transesophageal Doppler color flow mapping. in American heart journal 1991
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TGF-beta1 does not affect HBV duplication in HepG2.2.15 cells and can inhibit the expression of HBsAg and HBeAg. TGF-beta1 can downregulate the mRNA expression of SOCS-3 and upregulate the mRNA expression of SREBP-1c.
These observations are consistent with a model in which the loss of Dkk-3 in prostate cancer leads to increased secretion of TGFBI and ECM-1, which have tumor-promoting and tumor-protective roles, respectively
the involvement of ATF3 and its splice variant DeltaZip2 in TGF-b1 and Nrf2-driven pancreatic tumorigenesis was investigated. As demonstrated here, PDAC cells or premalignant H6c7 pancreatic ductal epithelial cells differentially express DeltaZip2- and ATF3, relating to stronger Nrf2 activity seen in Panc1 cells and TGF-ss1 activity in T3M4 or H6c7 cells, respectively.
Proatherogenic risk factor for lower-limb Peripheral Arterial Disease in Russian population is an increase of TGFbeta1 secretion without genetic predisposition.
Hepatitis B virus and Hepatitis C virus affect the association between TGF-beta1 C-509T variants and hepatocellular carcinoma susceptibility in opposite manners (Meta-Analysis).
results suggest that head and neck squamous cell carcinoma patients who exhibit persistently elevated soluble MICA and TGF-beta1 levels after chemoradiotherapy are at higher risk of tumor progression or death
These results suggest that Angiotensin II induces CTGF expression and extracellular matrix accumulation through a special TGF-beta-independent interaction between the NF-kappaB and Smad2/3 signals elicited by the AT1/PKCalpha/p38 MAPK pathway.
experiments demonstrated that the MYEOV ceRNA sequestered miR-30c-2-3p from binding its targets TGFBR2 and USP15 mRNAs, which in turn leading to constitutive activation of TGF-beta signaling and tumor progression in Non-small cell lung cancer.
human BAMBI may function as a molecular switch to control TGFbeta signalling strength and the Th17/Treg cell balance
eRF3b37 is thought to serve a role in hepatic stellate cells by inhibiting TGFbeta signaling.
This study strongly suggests dedifferentiation driven by TGF-beta signaling enhances stem cell properties in human colorectal cancer.
The expression of Pard3 was increased by the inhibition of miR-483, but TGF-beta1-induced cell migration and invasion were decreased by miR-483 inhibition. A dual-luciferase reporter assay determined that Pard3 expression was downregulated when targeted with miR-483. The epithelial-mesenchymal transition (EMT), as well as Tiam1-Rac signaling, was induced by TGF-beta1, which was decreased by the overexpression of Pard3.
These results suggest that nuclear c-Abl-mediated tyrosine phosphorylation of TIF1gamma has a desuppressive role in TGF-beta-Smad2/3 signaling.
TGF-beta promotes the migration and invasion abilities of breast cancer cells, along with the increase in EGFR expression.
SPARC knockdown partially eliminated TGFB1 function in inducing EMT of A549 cells. SPARC follistatin-like functional domain reduced the expression of E-cadherin, but had no effect on the expression of p-Akt and p-ERK
Rapamycin-insensitive mTORC1 signaling via 4E-BP1 is a critical pathway for TGF-beta1 stimulated collagen synthesis in human lung fibroblasts, whereas canonical PI3K/Akt signaling is not required.
These data suggested that decreased TGFB1 methylation may contribute to the development of autism spectrum disorder .
Studies suggest the therapeutic potentials of targeting the transforming growth factor-beta (TGF-beta) pathway in cancer [Review].
The AA genotype of rs1800470 in TGFB1 was associated with the multibacillary leprosy form in the start population, and this association was confirmed for the replication population.
TGF-B1rs1982073 polymorphism at the miRNA-187 binding site combined with HPV16 L1 seropositivity is associated with a joint effect on oropharyngeal squamous cell carcinoma susceptibility.
TGF-beta1 stimulated lubricin secretion by superficial zone chondrocytes at all densities with twice-a-week TGF-beta treatment. It is noteworthy that the daily treatment of TGF-beta1 increased lubricin much higher compared with twice-a-week treatment.
hypoxia increased the expression of platelet-derived growth factor (PDGF) and transforming growth factor-beta1 (TGF-beta1) and decreased the expression of neprilysin (NEP), which contributed to the hypoxia-induced Endothelial-to-mesenchymal transition of pulmonary artery endothelial cells.
TGF-beta1 modulates the expression of syndecan-4 in cultured vascular endothelial cells in a biphasic manner.
Taken together, Staphylococcus aureus induces TGF-beta1 and bFGF expression through the activation of AP-1 and NF-kappaB in bovine mammary gland fibroblasts.
localized to maternal septum in the interdigitation area of cotyledonary villi and caruncle
The results identify TGFB1 and ESRRA as likely transcriptional regulators of rumen epithelial development and energy metabolism, respectively, and provide targets for modulation of rumen development and function in the growing calf.
the combined treatment with TGF-beta1 and BMP-7 or treatment first with TGF-beta1 followed by BMP-7 was more effective than other treatment groups in both chondrogenic differentiation and SZP secretion.
Tenascin-X promotes activation of latent TGF-beta1 and subsequent epithelial to mesenchymal transition in mammary epithelial cells.
a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.
Endogenous TGF-beta1 became more bioactive following activation of the transgene protein product in chondrocytes.
A novel peptide, P2K, regulating TGF-beta1 signaling had an anabolic effect on bovine intervertebral disc cells and rabbit degenerated discs.
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.
Role of TGF-beta1 and TNF-alpha in IL-1beta mediated activation of proMMP-9 in pulmonary artery smooth muscle cells: involvement of an aprotinin sensitive protease.
Immunohistochemistry in rectus abdominis muscle from foetuses at 180 and 260 days post-conception
vascular endothelial growth factor indirectly stimulates smooth muscle cell proliferation and migration through the modulation of basic fibroblast growth factor and transforming growth factor beta(1) released by endothelial cells
Data show that as antral follicles develop, transforming growth factor (TGF)-beta3 is the most abundant TGF-beta isoform and TGF-beta1 protein levels decline in large follicles.
TGF-beta 1 signaling pathway controls pericyte growth state and contractile phenotype
Reactive oxygen species mediate TGF-beta1-induced TIMP-3 gene expression
MGP plays a role in endothelial cell function, by increasing transforming growth factor-beta1 activity and stimulating VEGF expression
Exogenous TGF-beta1, IGF-I, EGF and GH inhibited fetal bovine serum-deficiency-stimulated TGF-beta1 expression in mammary epithelium.
TGFB1overexpressing bone marrowderived mesenchymal stem cells promoted new bone formation in the rabbit femoral defect model.
Data indicate that cardiac contractility modulation (CCM) therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-beta1/Smad3 signaling pathway in chronic heart failure .
Studied effects of panax notoginseng saponins on the differentiation of mesenchymal stem cells using gene silencing of TGF-B1 signal pathway.
study suggested that TGF-beta1/Smad3/smad7 is a major pathway which plays an important role in the regulation of the IUA and specific inhibitor of Smad3 (SIS3) may provide a new therapeutic strategy for IUA.
cell therapy promoted TGF-beta1 expression in nucleus pulposus, leading to anti-inflammatory effects via the inhibition of NF-kappaB, and the amelioration of disc degradation.
that prenatal tracheal occlusion increases TGF-beta/Rho kinase pathway, myofibroblast differentiation, and matrix deposition in neonatal rabbit and human congenital diaphragmatic hernia lungs
observation. Based on the above results, we conclude that TGF-beta1-immobilized PLGA-gelatin scaffold seeded with ASCs considerably enhances the quality of the tissue-engineered cartilage, therefore, advancing the field of cartilage tissue engineering
Smad7 plays a crucial role in antagonizing epithelial-mesenchymal transition induced by TGFbeta signaling and is a Notch signaling target in limbal epithelial stem cells.
the role of IL-10 in inhibited allograft rejection may be associated with CD4+CD25+ regulatory T cells and IL-10, and may be independent of TGF-b
After NOTCH1 knockdown and TGFB1 stimulation, rabbit mesenchymal stem cells expressed higher levels of proteoglycan and collagen II.
Adverse biventricular remodeling in isolated right ventricular hypertension is mediated by increased transforming growth factor-beta1 signaling.
TGF-beta1 gene transcription significantly correlates with the surgical vaginal and dermal wound closure rate.
Wound closure was significantly protracted (P < 0.02), whereas TGFbeta1 gene expression was significantly increased (P < 0.0001) during the wound healing process in oophorectomised rabbits.
Radix astragali injection inhibits fibroblast proliferation in hypertrophic scars through down-regulating mRNA expression and protein synthesis of TGF-beta and Smad3.
Report established neointimal hyperplasia in vein grafts expands via TGF-beta1 (TGFB1)-mediated progressive fibrosis.
Thrombomodulin downregulation in vein gafts is mediated by paracrine release of TGF-beta1 caused by pressure-induced vessel stretch.
Angiotensin-(1-7) attenuates postangioplasty collagen synthesis in rabbits possibly through down-regulating the expression of TGF-beta1 and inhibiting the activation of Smad2 pathway.
TGF-beta1 may not be the primary mediator of muscle fibrosis in distraction osteogenesis
Glucosamine hydrochloride treatment can can partially decrease the expression levels of IL-1 beta and increase the expression levels of TGF-beta 1, which delays the development of osteoarthritis.
TGF beta is involved in the pathogenesis of tympanosclerosis.
There was significantly higher expression of TGF-beta1 and MMP-9 in nasal mucosa of experimental allergic rhinitis guinea pigs than in controls.
TGF-beta1 regulated pAKT and IFNgamma expressions were associated with epithelial cell survival in rhesus macaque colon explants and suggest a potential role of mucosal TGF-beta1 in regulating intestinal homeostasis and EC integrity.
T allele of the 29C>T polymorphism in the transforming growth factor-beta1 gene might be a risk factor of sarcopenia in a Japanese population.
SIV infection of rhesus macaques results in the emergence of IL-17-expressing cells during the acute phase. This subpopulation appears at day 14 postinfection concomitantly with an increase in TGF-beta and IL-18 expression.
SIV-infected macaques exhibiting progression to AIDS displayed greater expression of TGF-beta and indoleamine 2,3 dioxygenase in CD8+ T cells from mesentric lymph nodes.
TGFB1 can inhibit Salmonella replication whereas TRP53 can promote Salmonella replication in porcine peripheral blood mononuclear cells and murine macrophages.
TGF-beta1 is activated or inactivated by MMP20 or KLK4 and that the amelogenin cleavage product is necessary for the in-solution mobility of TGF-beta1.
Activated TGF-beta signaling rescued miR-143-reduced FSHR and intracellular signaling molecules, and miR-143-induced porcine granulosa cell apoptosis.
TGF-beta1-induced epithelial-myofibroblast plasticity is FAK- dependent, whereas TGF-beta1-induced apoptosis is favored when FAK signaling is inhibited.
this study shows that TGF-beta1 protects intestinal integrity and influences Smad and MAPK signal pathways in intestinal epithelium cells after TNF-alpha challenge
this study shows that anemonin may ameliorate LPS-induced intestinal injury and improve restoration by regulating the TGF-b1 and EGFR signaling pathways
The results indicated that TGF-beta-1 was associated with the restoration of intestinal morphology and barrier function following weaning stress.
Data (including data from in vitro and in vivo experiments) suggest that day 14 elongated conceptus secretes proteins that up-regulate TGFbeta1 mRNA and TGFbeta1 expression in endometrium; TGFbeta1 may be important during pregnancy maintenance.
The effects of semen, spermatozoa in extender, or extender alone on the expression of TGF-beta1, IL-10, and IL-6 in ovarian follicles are reported.
Dietary (1,3/1,6)-beta-D-glucan reduced the mRNA expression of transforming growth factor (TGF) beta2 and tended to reduce the mRNA expression of TGF-beta1 in lung tissue of neonatal piglet.
TGF-beta1, via TGF-beta1 receptor I and p38 MAPK signaling, reduces CFTR expression to impair CFTR-mediated anion secretion, which would likely compound the effects associated with mild CFTR mutations and ultimately would compromise male fertility.
High yield isolation of BMP-2 from bone and in vivo activity of a combination of BMP-2/TGF-beta1.
Boar seminal plasma contained TGF- beta1 and IL-10 but with high individual variation.
The present study was aimed to determine the association between metalloproteinase 3 (MMP3), transforming growth factor beta 1 (TGFbeta1) and collagen type X alpha I (COL10A1) gene polymorphisms with traits related to leg weakness in pigs.
Inhibition of transforming growth factor beta-1 augments liver regeneration after partial portal vein ligation in a porcine experimental model.
TGF-beta prevents excessive heart valve growth under normal physiological conditions while it promotes cell proliferation in the early stages of repair.
Crystals of dimeric porcine proTGF-beta1 reveal a ring-shaped complex, a novel fold for the prodomain, and show how the prodomain shields the growth factor from recognition by receptors and alters its conformation.
The effects of different polymorphisms of TGF-beta1 on litter size in Large white pigs are reported.
TGF-beta disrupts an IGF-II-stimulated autocrine amplification cascade that is necessary for muscle differentiation in vitro.
beta-Catenin plays a critical role in mediating TGF-beta1-induced myofibroblast differentiation in aortic valve interstitial cells.
Together, our results point to TGF-beta1 signaling pathway as a potential mediator of the radial glia-endothelial cell interactions and shed light to the key role of radial glia in paving the brain vascular network.
Hypothalamic TGF-beta1 down-regulation attenuates hypothalamic inflammation and improves energy metabolism, resulting in lower body-mass gain and lower fat-mass accumulation, which protects mice from the development of obesity.
High amounts of TGF-beta in the eye cause a substantial reduction in the activity of Wnt/beta-catenin signaling. This effect is inhibited in the presence of high amounts of Norrin, which further induce the expression of SMAD7 to inhibit TGF-beta signaling.
platelet TGF-beta1 partially contributes to liver fibrosis, most likely by initiating profibrotic signaling in hepatic stellate cells and collagen synthesis.
We have demonstrated an essential role of IL-7 and TGF-beta in the generation of thymus-derived Tregs in the co-culture of thymocytes and JAWS II cells. In addition, in vitro generated Tregs exhibited their suppressive function similarly to Tregs sorted from freshly isolated thymus.
transcriptional regulator Meox1 controls TGF-beta-induced SMC differentiation from mesenchymal progenitor cells by preventing PPM1A-mediated Smad3 dephosphorylation
These results show that the levels of AMTN mRNA induced by TGFbeta1 and Smad3 are decreased by robust expression of Bax in gingival epithelial cells.
High TGFB1 expression is associated with pulmonary fibrosis.
this paper shows that epithelial-derived TGF-beta1 acts as a pro-viral factor in the lung during influenza A infection
Study points toward elevated levels of active TGF-beta as inducers and promoters of ectopic bone formation, and suggest that TGF-beta might be a therapeutic target in heterotopic ossification.
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.
Genetic or pharmacologic inactivation of SHP2 promotes accumulation of JAK2 phosphorylated at Y570, reduces JAK2/STAT3 signaling, inhibits TGFbeta-induced fibroblast activation and ameliorates dermal and pulmonary fibrosis.
Results indicate that the miR-23a cluster regulates osteocyte differentiation by modulating the TGF-beta signalling pathway.
SOX9 was over-expressed in liver after ischemia/reperfusion injury. Suppressing SOX9 markedly reduced the inflammatory response. Also, transforming growth factor (TGF)-beta1 was highly induced in liver after ischemia/reperfusion injury.
Following Schistosoma exposure, TSP-1 levels in the lung increase, via recruitment of circulating monocytes, while TSP-1 inhibition or knockout bone marrow prevents TGF-beta activation and protects against pulmonary hypertension development.
TGF-beta/Smad proteins signaling affects radiation response and prolongs survival by regulating DNA repair genes in malignant glioma.
The results indicate that EGFR and its activation are critical for YAP-mediated suppression of TGF-beta1-induced apoptosis. This study provides a new understanding of the regulatory mechanism underlying the determination of cell fate in response to TGF-beta1-mediated simultaneous apoptosis and epithelial mesenchymal transformation.
transforming growth factor beta (TGFbeta) signaling was upregulated in HSCs from bone marrow of mice with MLL-AF9-induced acute myeloid leukemia (AML) because of excessive production of TGFbeta1, especially from megakaryocytes, and overactivation of latent TGFbeta1 protein.
TGF-beta release from platelets is necessary for podoplanin-mediated tumor invasion and metastasis in lung cancer.
Data suggest partial or complete transforming growth factor beta 1 (TGFBI) knockdown as a potential therapy against TGFBI-linked corneal dystrophies.
This gene encodes a member of the transforming growth factor beta (TGFB) family of cytokines, which are multifunctional peptides that regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types. Many cells have TGFB receptors, and the protein positively and negatively regulates many other growth factors. The secreted protein is cleaved into a latency-associated peptide (LAP) and a mature TGFB1 peptide, and is found in either a latent form composed of a TGFB1 homodimer, a LAP homodimer, and a latent TGFB1-binding protein, or in an active form composed of a TGFB1 homodimer. The mature peptide may also form heterodimers with other TGFB family members. This gene is frequently upregulated in tumor cells, and mutations in this gene result in Camurati-Engelmann disease.
TGF-beta 1 protein
, latency-associated peptide
, transforming growth factor beta-1
, transforming growth factor, beta 1 (Camurati-Engelmann disease)
, transforming growth factor-beta 1
, transforming growth factor beta 1
, transforming growth factor-beta
, transforming growth factor beta1
, transforming growth factor-beta-1
, TGF-beta 1
, regulatory protein
, transforming growth factor, beta-1