Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human TGFB1 Antibodies:
anti-Mouse (Murine) TGFB1 Antibodies:
anti-Rat (Rattus) TGFB1 Antibodies:
Go to our pre-filtered search.
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 Polyclonal TGFB1 Primary Antibody for IF, IHC - ABIN6711930
Yoshioka, Tsujihata, Akanae, Nonomura, Okuyama: Angiotensin type-1 receptor blocker candesartan inhibits calcium oxalate crystal deposition in ethylene glycol-treated rat kidneys. in Urology 2011
Show all 13 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 10 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 Polyclonal TGFB1 Primary Antibody for WB - ABIN6688644
Zhao, Yin, Li, Fan, Yang, Chen, Wang: MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice. in Aging cell 2017
Show all 7 Pubmed References
Human Polyclonal TGFB1 Primary Antibody for WB - ABIN6149071
Xie, Chen, Hu, Pan, Wang, Li, Geng, Xu: Premature senescence of cardiac fibroblasts and atrial fibrosis in patients with atrial fibrillation. in Oncotarget 2017
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 6 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 6 Pubmed References
Peritoneal membrane damage in patients on peritoneal dialysis is associated with fibrosis and neoangiogenesis through the TGF-beta1-VEGF-A pathway.
TGF levels were significantly higher in the cavernous compartment than in the systemic blood. A linear decrease was evident in the cavernous blood when the flaccid penis became tumescent (24.3 +/- 14.5 to 13.9 +/- 6.5) and rigid (to 8.7 +/- 3.1). At detumescence, TGF increased to 18.3 +/- 10.4. In contrast, the levels in the systemic circulation remained unchanged.
Carriers of A-allele genotypes of the IL10 -1080A/G SNP had significantly lower CD83+ cells (p = 0.046) in the tumor invasive margin. The T-allele of the TGFB1 -509C/T SNP might be a protective factor for development of CRC, although, in the course of the disease, this variant allele might be associated with more unfavorable prognosis of the patients.
PSPC1 increases transforming growth factor-beta1 (TGF-beta1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-beta1 autocrine signaling, promoting epithelial mesenchymal transformation, stemness and metastasis.
Particulate matter 2.5 induces the expression of TGF-beta1, PDGF-AB, and PDGF-BB in vitro via HMGB1-RAGE signaling, suggesting that this pathway may contribute to the airway remodeling observed in patients with chronic obstructive pulmonary disease.
The results demonstrated that TGF-beta1 plays a crucial role in the Desmoid-like fibromatosis (DF) cells growth and, together with cell-cell interactions, in DF myofibroblast conversion; we also highlighted that the cellular sensitivity to this cytokine was an intrinsic feature of the DF cells.
Pulmonary levels of TGF-beta1 during the first week of acute respiratory distress syndrome were not associated nor with the presence of fibroproliferation neither with death.
This finding reveals how GARP exploits an unusual medley of interactions, including fold complementation by the amino terminus of TGF-beta1, to chaperone and orient the cytokine for binding and activation by alphaVbeta8.
In regards to extracellular matrix remodelling, treprostinil significantly reduced PDGF-BB-TGF-beta1-CTGF induced synthesis and deposition of collagen type I and fibronectin, in a cAMP sensitive manner
The data show that TGFB1 induces THBS1 expression via Smad3 which contributes to the invasive behavior during glioblastoma multiforme expansion.
beta-TrCP1 isoforms interact with CENP-W with different binding preferences.
TGFbeta mediated LEFTY/Akt/GSK-3beta/Snail axis may contribute to the establishment and maintenance of phenotypic characteristics of ovarian clear cell carcinoma through modulation of epithelial-mesenchymal transition /Cancer Stem Cell properties.
Our findings strengthen the association of TGFB1 (rs1800472) with otosclerosis and support a relationship between RELN and familial otosclerosis only, which may explain previous variable replications.
findings revealed that S100A11 and TGF-beta1/SMAD4 signaling pathway were related but mutually independent in regulating PANC-1 cells proliferation and apoptosis.
an unconventional secretion mode of TGFB1 adding another level of control of its bioavailability and activity in order to effectively orchestrate cellular programs prone to dysregulation as seen in fibrosis and cancer
This observation provides new insights into the potential role of TGF-beta in the redox regulation of thyroid cells.
genotype G/G and genotypes G/C and C/C at codon 25 of TGF-beta1 seemed to confer resistance and susceptibility to the development of American tegumentary leishmaniasis, respectively, in the sample population assessed in this study.
The data demonstrate that c.74G>C and c.29C>T polymorphisms in the TGFB1 signal peptide are significantly associated with risk of human papillomavirus infection and high-grade squamous intraepithelial lesions, respectively.
These findings suggested the potential protective role of miR-217 on the attenuation of cell proliferation and migration was through targeting ZEB1 in TGF-beta1-stimulated airway smooth muscle cells.
the diagnostic power of TGF-beta and blood inflammatory parameters in the prediction of intraperitoneal adhesions in obese patients undergoing second surgical intervention, was determined.
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.
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.
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 serves as a vegetally enriched, intrinsic factor 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
sortilin 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 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.
The TGF-beta1 mRNA was the highest expressed member of the TGFbeta super family in cartilage. TGF-beta1 promoted functional gap junction intercellular communication through increased expression of Cx43.
The differentiation of mucosal langerhans cells (LCs) is a two-step process. In the lamina propria, signaling via BMP7-ALK3 promotes translocation of LC precursors to the epithelium. Within the epithelium, TGF-beta1 finalizes LC differentiation, and ALK5 is crucial to this process.
Wnt5a promotes kidney fibrosis by stimulating Yap/Taz (Wwtr1)-mediated macrophage M2 polarization
These studies provide evidence that elevated levels of TGFbeta signaling may contribute to the disease phenotype of cherubism and a reduction in pathway activity may be an effective therapeutic approach to treat this rare disease.
TGFbeta1 could stimulate mTORC2 and Yap/Taz activation in NRK-49F 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.
Peripheral neuropathies can result from damage or dysregulation of the insulating myelin sheath surrounding spinal motor axons, causing pain, inefficient nerve conduction, and the ectopic migration of oligodendrocyte progenitor cells (OPCs), the resident myelinating glial cell of the CNS, into the periphery.
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.
TGFbeta1a regulates zebrafish posterior lateral line formation via Smad5 mediated pathway.
PCSK7 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 suppresses TGF-beta signaling by physically associating with Smad4 and preventing the formation of Smad2/3/4 and Smad1/5/9/4 complexes
TGF-beta1 acts at multiple sites, including LH receptor, 20beta-HSD and membrane progestin receptor-beta, to inhibit zebrafish oocyte maturation
These data suggest Pez plays a crucial role in organogenesis by inducing TGFbeta and epithelial-mesenchymal transition.
Data show that Rock2 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