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anti-Human TGFB1 Antibodies:
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Various Species Monoclonal TGFB1 Primary Antibody for CyTOF, ELISA (Capture) - ABIN4900860
Phillips: Rapid analysis of inflammatory cytokines in cerebrospinal fluid using chip-based immunoaffinity electrophoresis. in Electrophoresis 2004
Show all 50 Pubmed References
Human Polyclonal TGFB1 Primary Antibody for IF (p), IHC (p) - ABIN724685
Kou, Hu, Yao, Wang, Shen, Kang, Hong: Transforming growth factor-?1 promotes Treg commitment in nasal polyposis after intranasal steroid treatment. in Inflammation research : official journal of the European Histamine Research Society ... [et al.] 2013
Show all 15 Pubmed References
Human Monoclonal TGFB1 Primary Antibody for FACS - ABIN4898892
Yamauchi, Ueki, Konno, Ito, Takeda, Nakamura, Nishikawa, Moritoki, Omokawa, Saga, Hirokawa: The effect of hepatocyte growth factor on secretory functions in human eosinophils. in Cytokine 2016
Show all 8 Pubmed References
Human Monoclonal TGFB1 Primary Antibody for FACS - ABIN4897280
Azukizawa, Döhler, Kanazawa, Nayak, Lipp, Malissen, Autenrieth, Katayama, Riemann, Weih, Berberich-Siebelt, Lutz: Steady state migratory RelB+ langerin+ dermal dendritic cells mediate peripheral induction of antigen-specific CD4+ CD25+ Foxp3+ regulatory T cells. in European journal of immunology 2011
Show all 7 Pubmed References
Human Polyclonal TGFB1 Primary Antibody for WB - ABIN223608
Tamaki, Hatano, Taura, Tada, Kodama, Nitta, Iwaisako, Seo, Nakajima, Ikai, Uemoto: CHOP deficiency attenuates cholestasis-induced liver fibrosis by reduction of hepatocyte injury. in American journal of physiology. Gastrointestinal and liver physiology 2008
Show all 6 Pubmed References
Human Monoclonal TGFB1 Primary Antibody for CyTOF, FACS - ABIN4900169
Boswell, Sharif, Alisa, Pereira, Williams, Behboudi et al.: Induction of latency-associated peptide (transforming growth factor-β(1)) expression on CD4+ T cells reduces Toll-like receptor 4 ligand-induced tumour necrosis factor-α production in a transforming ... in Immunology 2011
Show all 5 Pubmed References
Human Monoclonal TGFB1 Primary Antibody for ELISA, FACS - ABIN4359062
Makboul, Makboul, Abdelhafez, Hassan, Youssif: Evaluation of the effect of fractional CO2 laser on histopathological picture and TGF-β1 expression in hypertrophic scar. in Journal of cosmetic dermatology 2014
Show all 4 Pubmed References
Mouse (Murine) Monoclonal TGFB1 Primary Antibody for CyTOF, FACS - ABIN4899119
Lee, Park, Woo, Park, Kang et al.: RhoA/phosphatidylinositol 3-kinase/protein kinase B/mitogen-activated protein kinase signaling after growth arrest-specific protein 6/mer receptor tyrosine kinase engagement promotes epithelial cell ... in The Journal of pharmacology and experimental therapeutics 2014
Show all 4 Pubmed References
Human Polyclonal TGFB1 Primary Antibody for ELISA, ICC - ABIN4359055
Barsby, Guest: Transforming growth factor beta3 promotes tendon differentiation of equine embryo-derived stem cells. in Tissue engineering. Part A 2013
Show all 3 Pubmed References
Human Monoclonal TGFB1 Primary Antibody for EIA, Func - ABIN114558
Crawford, Stellmach, Murphy-Ullrich, Ribeiro, Lawler, Hynes, Boivin, Bouck: Thrombospondin-1 is a major activator of TGF-beta1 in vivo. in Cell 1998
Show all 4 Pubmed References
The present study demonstrated that in human osteoarthritis fibroblastlike synoviocytes, TGF-beta signals via p-Smad2 (show SMAD2 Antibodies) and p-Smad1 (show GARS Antibodies)/5/8. Furthermore, it was demonstrated that LTBP-1 (show LTBP1 Antibodies) may modulate the activity of TGF-beta in human osteoarthritis fibroblastlike synoviocytes.
These data indicate that human amniotic epithelial cells (hAECs) endow potential anticancer properties on epithelial ovarian cancer in vivo and in vitro which is partially mediated by hAECsecreted TGFbeta1-induced cell cycle arrest. This study suggests a potential application of hAECbased therapy against epithelial ovarian cancer.
Results demonstrated that TGF-beta1 regulated FUT1 and Lewis y expression by activating the MAPK/c-Fos pathway.
analysis of how the molecular mechanisms involved in the dual response to TGF-beta in cancer, and how tumor cells evolve to evade the tumor-suppressive responses of this signaling pathway and then hijack the signal, converting it into an oncogenic factor [review]
The present study demonstrated that the expression of LKB1 (show STK11 Antibodies) and SIK1 (show SIK1 Antibodies) was downregulated, while TGF-beta and epithelialmesenchymal transition protein expression levels were upregulated in clinical ovarian tumor tissues and cells.
TGFB1 was shown to induce Epithelialtomesenchymal transition, thereby promoting the migration and invasion of HepG2 cells via JAK (show JAK3 Antibodies)/STAT3 (show STAT3 Antibodies)/Twist signaling.
Expression of TGF-beta was closely related to hypertrophy of the ligamentum flavum.
lasma levels of all TGF-beta isoforms were not altered in adolescent Chronic fatigue syndrome.
these results indicated that Bone marrow-derived mesenchymal stem cells -conditioned medium suppressed the epithelial-mesenchymal transition which might be associated with TGF-B1/Smad3 (show SMAD3 Antibodies). This study provides the theoretical basis for the research of the mechanisms responsible for pulmonary disease.
we show that NORAD upregulates transforming growth factor-beta (TGF-beta) signaling and regulates TGF-beta-induced epithelial-to-mesenchymal transition (EMT (show ITK Antibodies))-like phenotype
TGF-beta1 stimulated lubricin (show PRG4 Antibodies) 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 (show PRG4 Antibodies) much higher compared with twice-a-week treatment.
hypoxia increased the expression of platelet-derived growth factor (PDGF (show PDGFA Antibodies)) and transforming growth factor-beta1 (TGF-beta1) and decreased the expression of neprilysin (NEP (show MME Antibodies)), which contributed to the hypoxia-induced Endothelial-to-mesenchymal transition of pulmonary artery endothelial cells.
TGF-beta1 modulates the expression of syndecan-4 (show SDC4 Antibodies) in cultured vascular endothelial cells in a biphasic manner.
Taken together, Staphylococcus aureus induces TGF-beta1 and bFGF (show FGF2 Antibodies) expression through the activation of AP-1 (show JUN Antibodies) and NF-kappaB (show NFKB1 Antibodies) in bovine mammary gland fibroblasts.
The results identify TGFB1 and ESRRA (show ESRRA Antibodies) 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 (show BMP7 Antibodies) or treatment first with TGF-beta1 followed by BMP-7 (show BMP7 Antibodies) was more effective than other treatment groups in both chondrogenic differentiation and SZP (show PRG4 Antibodies) secretion.
Tenascin-X (show TNXB Antibodies) 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 (show SMAD1 Antibodies)/5/8 and Smad2 (show SMAD2 Antibodies)/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 Antibodies).
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 indicate that cardiac contractility modulation (CCM) therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-beta1/Smad3 (show SMAD3 Antibodies) signaling pathway in chronic heart failure .
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 (show NFKB1 Antibodies), and the amelioration of disc degradation.
that prenatal tracheal occlusion increases TGF-beta/Rho kinase (show ROCK1 Antibodies) 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 (show SMAD7 Antibodies) plays a crucial role in antagonizing epithelial-mesenchymal transition induced by TGFbeta signaling and is a Notch (show NOTCH1 Antibodies) 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 (show NOTCH1 Antibodies) knockdown and TGFB1 stimulation, rabbit mesenchymal stem cells expressed higher levels of proteoglycan (show Vcan Antibodies) and collagen II.
TGF-beta1 gene transcription significantly correlates with the surgical vaginal and dermal wound closure rate.
TGF beta is involved in the pathogenesis of tympanosclerosis.
There was significantly higher expression of TGF-beta1 and MMP-9 (show MMP9 Antibodies) in nasal mucosa of experimental allergic rhinitis guinea pigs than in controls.
TGF-beta1 regulated pAKT (show AKT1 Antibodies) 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.
SIV infection of rhesus macaques results in the emergence of IL-17 (show IL17A Antibodies)-expressing cells during the acute phase. This subpopulation appears at day 14 postinfection concomitantly with an increase in TGF-beta and IL-18 (show IL18 Antibodies) expression.
SIV-infected macaques exhibiting progression to AIDS displayed greater expression of TGF-beta and indoleamine 2,3 dioxygenase in CD8 (show CD8A Antibodies)+ T cells from mesentric lymph nodes.
TGF-beta1 is activated or inactivated by MMP20 or KLK4 (show KLK4 Antibodies) and that the amelogenin (show AMELX Antibodies) cleavage product is necessary for the in-solution mobility of TGF-beta1.
Activated TGF-beta signaling rescued miR (show MYLIP Antibodies)-143-reduced FSHR (show FSHR Antibodies) and intracellular signaling molecules, and miR (show MYLIP Antibodies)-143-induced porcine granulosa cell apoptosis.
TGF-beta1-induced epithelial-myofibroblast plasticity is FAK (show PTK2 Antibodies)- dependent, whereas TGF-beta1-induced apoptosis is favored when FAK (show PTK2 Antibodies) signaling is inhibited.
this study shows that TGF-beta1 protects intestinal integrity and influences Smad (show SMAD1 Antibodies) and MAPK (show MAPK1 Antibodies) signal pathways in intestinal epithelium cells after TNF-alpha (show TNF Antibodies) challenge
this study shows that anemonin may ameliorate LPS (show IRF6 Antibodies)-induced intestinal injury and improve restoration by regulating the TGF-b1 and EGFR (show EGFR Antibodies) 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 (show IL10 Antibodies), and IL-6 (show IL6 Antibodies) in ovarian follicles are reported.
Dietary (1,3/1,6)-beta-D-glucan reduced the mRNA expression of transforming growth factor (TGF) beta2 (show TGFB2 Antibodies) 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 (show MAPK14 Antibodies) signaling, reduces CFTR (show CFTR Antibodies) expression to impair CFTR (show CFTR Antibodies)-mediated anion secretion, which would likely compound the effects associated with mild CFTR (show CFTR Antibodies) mutations and ultimately would compromise male fertility.
These data indicate that TGF-beta signaling is crucial for the function of the transition zone, which in turn may affect the regulation of cilia length.
R-Smads are the key components of TGFbeta beta signals in germ layer induction. SCP3 (show SYCP3 Antibodies) serves as a vegetally enriched, intrinsic factor (show GIF Antibodies) to ensure a prepared status of Smads for their activation.
the present in vitro system, which permits not only the cell contraction-mediated cell sorting but also the TGF-b-directed mesodermal induction such as cartilage formation, may fairly reflect the embryogenesis in vivo.
Loss of XTgfbi impaired blastopore formation and dorsal tissue morphogenesis.
TGF-beta signaling has a role in nuclear localization of transcription factor Smad4 (show SMAD4 Antibodies)
sortilin (show SORT1 Antibodies) negatively regulates TGF-beta signaling by diverting trafficking of precursor proteins to the lysosome during transit through the biosynthetic pathway
Within the limitations of the study design, production of COMP (show COMP Antibodies) during healing of skin wounds does not appear to be influenced by wound type or anatomic site, nor does it appear to be correlated with TGF-beta1 concentrations.
Peritoneal TGF-beta(1) concentration was higher in horses with severe gastrointestinal diseases, in horses with an altered peritoneal fluid, and in nonsurvivors.
In obese mice, periodontitis caused the downregulation of MMP2 (show MMP2 Antibodies), and upregulation of TIMP1 (show TIMP1 Antibodies) and TGF-beta1 at transcriptional and translational levels
The protective effect of the EP2 receptor on TGF-beta1 induced podocyte injury via the PI3K / Akt (show AKT1 Antibodies) signaling pathway.
This study demonstrates that prevention of renal apoB (show APOB Antibodies) accumulation is a mechanism by which TGF-beta inhibition is nephroprotective.
data show that increased TGFbeta in the tumour microenvironment represents a primary mechanism of immune evasion that promotes T-cell exclusion and blocks acquisition of the TH1 (show HAND1 Antibodies)-effector phenotype; immunotherapies directed against TGFbeta signalling may therefore have broad applications in treating patients with advanced colorectal cancer
IL 6 (show IL6 Antibodies) and TGF beta perform essential role in cerebral malaria pathogenesis by modulating the level of glial cell induced neuroinflammation.
The increased susceptibility to IMQ-induced psoriasis of GILZ (show TSC22D3 Antibodies)-Tg mice was significantly associated with skin-specific over-activation of TGF-beta1-mediated signaling via SMAD2 (show SMAD2 Antibodies)/3.
The data suggest that B cells can down-regulate the function of antigen-presenting cells, and in turn encephalitogenic Th1 (show HAND1 Antibodies)/Th17 responses, via TGF-beta1.
p-SMAD2 (show SMAD2 Antibodies)/3 and p-ERK1/2 might play a regulatory role in TGF-beta1 induced CTGF (show CTGF Antibodies) exp p-SMAD2 (show SMAD2 Antibodies)/3 and p-ERK1/2 might play a regulatory role in TGF-beta1 induced CTGF (show CTGF Antibodies) expression during tooth development.
inhibiting NCAM1 (show NCAM1 Antibodies) would be cardioprotective, counteract the pathological action of TGFbeta1 and reduce heart failure severity.
TGF-beta signaling has a role in inhibiting tumor progression and invasion in an induced mouse bladder cancer model
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...
The fine tuning of TGF-beta signaling derives from positive and negative control by Ldb2a (show LDB2 Antibodies).
TGFbeta1a regulates zebrafish posterior lateral line formation via Smad5 (show SMAD5 Antibodies) mediated pathway.
PCSK7 (show PCSK7 Antibodies) is essential for zebrafish development and regulates the expression and proteolytic cleavage of TGFbeta1a.
TGFbeta signaling orchestrates the beneficial interplay between scar-based repair and cardiomyocyte-based regeneration to achieve complete heart regeneration.
TGFbeta1 plays a role in zebrafish keratocyte migration.
data presented show that Zili (show PIWIL2 Antibodies) suppresses TGF-beta signaling by physically associating with Smad4 (show SMAD4 Antibodies) and preventing the formation of Smad2 (show SMAD2 Antibodies)/3/4 and Smad1 (show SMAD1 Antibodies)/5/9/4 complexes
TGF-beta1 acts at multiple sites, including LH receptor (show LHCGR Antibodies), 20beta-HSD (show HAL Antibodies) and membrane progestin receptor-beta (show PAQR8 Antibodies), to inhibit zebrafish oocyte maturation
These data suggest Pez (show PTPN14 Antibodies) plays a crucial role in organogenesis by inducing TGFbeta and epithelial-mesenchymal transition.
Data show that Rock2 (show ROCK2 Antibodies) acts as a negative regulator of the TGFbeta signaling pathway.
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
, tgf-beta 5
, transforming gorwth factor-Beta5
, transforming growth factor-B5
, transforming growth factor-beta 5
, TGF-beta 1
, regulatory protein
, transforming growth factor, beta-1
, transforming growth factor, beta 1
, transforming growth factor, beta-induced, 68kDa
, transforming growth factor beta-1-like
, transforming growth factor beta 4
, TGF beta