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Our data uncover the ZEB1-miR-190-SMAD2 axis and provide a mechanism to explain the TGF-beta network in breast cancer metastasis.
MiR-128-3p overactivates the TGF-beta pathway in the non-small cell lung cancer cells.
TT genotype for TGFbeta C-509T had an increased risk and CC genotype for TGFbeta T869C had a decreased risk of gastric cancer in south Indian population
propose that a positive feedback mechanism between uPAR, plasmin and transforming growth factor beta1 (TGFbeta1) selects cells in the monolayer for matrix invasion
TGFbeta1 induces epithelial to mesenchymal morphology transition in TGFbeta1 sensitive non-small cell lung cancer (NSCLC) lines but not in insensitive lines. TGFbeta1 not only increases the mesenchymal maker Vimentin expression, but also enhances NSCLC cell invasiveness. TGFbeta1 elevates both the expression level of cancer stem-like cell markers and anchorage-dependent colony formation ability in TGFbeta1 sensitive l...
Despite the higher TGFbeta1 secretion it was not observed changes in the morphology or proliferation of epithelial cells when diabetes or hypertension was present
The results strongly suggest that the integrated pathway of TGF-beta/Snail with TNFalpha/NF-kappaB may be the principal axis that links cancer cells to their microenvironment during the epithelial-mesenchymal transition process and results in poor prognosis in colorectal cancer patients.
Although decreased TGF-beta1 and IL-35 plasma levels correlate positively with decreased vitamin D levels and negatively with severity of coronary artery disease, only TGF-beta1 has a significant association with vitamin D deficiency in CAD patients.
Findings suggest that glucocorticoids might be a useful therapy for preventing tissue remodeling by blocking the epithelial-to-mesenchymal transition initiated by TGF-beta1-induced MAPK and Snail/Slug signaling pathways in chronic rhinosinusitis with nasal polyps.
The present study highlights possible new molecular mechanisms involving progesterone, including inhibition of TGF-beta1-activated Smad signaling and TGF-beta1-regulated genes involved in bronchopulmonary dysplasia pathogenesis, which are likely to attenuate the development of BPD by inhibiting TGF-beta1-mediated airway remodeling.
We concluded that TGF-ss1-509C/T polymorphism was significantly associated with LC susceptibility, while the codon 10T/C polymorphism seemed to have a limited role in predicting the occurrence of LC induced by HBV/HCV infection.
In this review, regulatory interactions between fibulins and TGF-beta are discussed. Understanding biological roles of fibulins in TGF-beta regulation may introduce new insights into the pathogenesis of some human diseases. [review]
TGFbeta1 gene SNP rs1982073 might be correlated with congenital heart disease (CHD) susceptibility, and the T allele might decrease the disease risk. However, TGFbeta1 gene polymorphism rs1800471 was not related to CHD risk.
High TGFB1 expression is associated with idiopathic pulmonary fibrosis.
The heterozygous CT genotype of TGFB1 and its serum levels in Hashimoto's thyroiditis, is a genetic risk factor for developing a more severe form of Hashimoto's thyroiditis.
CTEN activated the expression of TGFB1, thereby prompting epithelial-mesenchymal transition in lung adenocarcinoma cancer cells.
blocking TGF-b signaling with the TGF-b receptor inhibitor SB431542 counteracted the effect of platelets on KLF6 expression and proliferation of HCC cells. Based on these findings, we conclude that platelet releasates, especially TGF-b, promote the proliferation of SMMC.7721 and HepG2 cells by decreasing expression of KLF6
Stimulation of cancer cells with TGFbeta1 weakened the ability of glioblastoma cells to attract hematopoietic stem cells (HSCs) and exchange a fluorescent tag. This process stimulated cancer cell proliferation, which is an indication of the ability of HSCs to 'switch' the proliferation and invasion processes in glioblastoma cells.
Long non-coding RNA 886 is induced by TGF-beta and suppresses the microRNA pathway in ovarian cancer.
these findings demonstrate that JunB and CBP-mediated histone hyperacetylation are responsible for TGF-beta1 induced ITGB6 transcription in oral squamous cell carcinoma (OSCC) cells, suggesting that epigenetic mechanisms are responsible for the active transcription expression of ITGB6 induced by TGF-beta1 in OSCC cells.
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.
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.
De novo formation of the biliary system by TGFbeta-mediated hepatocyte transdifferentiation
CXCL9 may promote prostate cancer progression via inhibition of cytokines from T cells.
EGCG attenuated airway inflammation in asthmatic mice, decreased the percentage of Th17 cells and increased the percentage of Treg cells. The antiinflammatory effect of EGCG is achieved via the TGFbeta1 signaling pathway.
fibrosis induced by Ang II may be alleviated by AKAP12 expression through inactivation of the TGF-beta1 pathway.
RUNX1 promoted TGF-beta-induced partial EMT by increasing transcription of the PI3K subunit p110delta, which mediated Akt activation.
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