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Gene Review

TGFB1  -  transforming growth factor, beta 1

Homo sapiens

Synonyms: CED, DPD1, LAP, TGF-beta-1, TGFB, ...
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Disease relevance of TGFB1

  • The transforming growth factor-beta1 (TGFB1) gene is associated with chronic obstructive pulmonary disease (COPD) [1].
  • Consecutive patients (n = 660) with breast cancer from the Memorial Sloan-Kettering Cancer Center (New York, NY) and healthy females (n = 880) from New York City were genotyped for the hypomorphic TGFBR1*6A allele and for the TGFB1 T29C variant that results in increased TGF-beta circulating levels [2].
  • We hypothesized that functional genetic variants in TGFB1 and TGFBR2 are associated with gastric cancer risk [3].
  • It suggests that Sp1, via transcriptional induction of vimentin, cooperates with activated Smad complexes in mesenchymal transition and migration of pancreatic cancer cells upon TGF-beta stimulation [4].
  • These studies suggest that the -509C and codon 10T, implicated in lower levels of TGF-beta1 protein production, are shared susceptibility factors associated with more severe granulomatous disease in sarcoidosis and CBD [5].
  • The aim of this paper is to review the possible value of TGF-beta1 as both a disease marker and a therapeutical target for cardiovascular disease [6].
  • Radiation failed to enhance lung metastases in mice bearing tumors that lack the type II TGF-beta receptor, suggesting that the increase in metastases was due, at least in part, to a direct effect of TGF-beta on the cancer cells [7].
  • Through its pleiotropic effects on these immune cells, TGF-beta prevents the development of autoimmune diseases without compromising immune responses to pathogens [8].
  • These results indicate that chronic inflammation associated with HCV infection shifts hepatocytic TGF-beta signaling from tumor-suppression to fibrogenesis, accelerating liver fibrosis and increasing risk for HCC [9].
  • In prostate cancer cell lines, TGF-beta-induced EMT was mediated by NF-kappaB signaling [10].
  • These data suggest that myofibroblasts in areas of fibrosis maintain their own phenotype through autocrine TGF-beta1 action and that extracellular HA matrices are an essential mediator of this [11].

Psychiatry related information on TGFB1


High impact information on TGFB1

  • IL-13 is the key effector cytokine in asthma and stimulates airway fibrosis through the action of matrix metalloproteinases on TGF-beta and promotes epithelial damage, mucus production, and eosinophilia [17].
  • These cells recognize antigen as do all T cells, but they secrete the immunoregulatory cytokines IL-10 and TGF beta [18].
  • TGF-beta 1 is produced by every leukocyte lineage, including lymphocytes, macrophages, and dendritic cells, and its expression serves in both autocrine and paracrine modes to control the differentiation, proliferation, and state of activation of these immune cells [19].
  • Increased production and activation of latent TGF-beta have been linked to immune defects associated with malignancy and autoimmune disorders, to susceptibility to opportunistic infection, and to the fibrotic complications associated with chronic inflammatory conditions [19].
  • IL-10 induces naive B cells to produce IgG3, IgG1, and IgA1, and further addition of TGF beta permits the secretion of IgA2 [20].

Chemical compound and disease context of TGFB1


Biological context of TGFB1


Anatomical context of TGFB1

  • The frequency of CD25 + memory CD4 + T cells and transient FOXP3 mRNA expression by CD4 + T cells significantly increased after systemic glucocorticoid treatment, whereas TGFB1 expression did not change [30].
  • In contrast, two pancreatic carcinoma cell lines, previously found to be growth stimulated by TGFB1, displayed an expression pattern opposite to that of these genes [29].
  • In this study, we have investigated whether cultures of cells from normal TA and PD plaques undergo osteogenesis, express markers for stem cells, and originate other cell lineages via processes modulated by TGFB1 [31].
  • EGF or TGFB1 alone stimulates but together attenuate granulosa cell DNA synthesis [32].
  • Overexpression of TGFB1 was found in the conditioned medium and cellular fractions of both hypertrophic keratinocytes and fibrotic fibroblasts [33].

Associations of TGFB1 with chemical compounds

  • TGFB1 expression was not affected by hyperhomocysteinaemia either in normal or in high glucose [34].
  • This study was designed for the histopathological, cellular and biochemical characterization of a skin lesion removed surgically from a young male several months after accidental exposure to cesium-137, with an emphasis on expression of transforming growth factor beta1 (TGFB1) and tumor necrosis factor alpha (TNFA) and the occurrence of apoptosis [33].
  • This result implicates serine/threonine phosphorylation as an important mechanism of TGF-beta receptor-mediated signaling [35].
  • This phenomenon of monocyte deactivation in septic patients with fatal outcome shows similarities to experimental monocytic refractoriness induced by LPS desensitization or by pretreatment with its endogenous mediators IL-10 and transforming growth factor-beta (TGF-beta) [36].
  • The latter appeared to be involved in the inhibition of proinflammatory cytokine production because addition of exogenous TGF-beta1, prostaglandin E2, or PAF resulted in inhibition of lipopolysaccharide-stimulated cytokine production [37].
  • Cholesterol-lowering agents (fluvastatin and lovastatin) and cholesterol-depleting agents (beta-cyclodextrin and nystatin) enhance TGF-beta responsiveness by increasing non-lipid raft microdomain accumulation of TGF-beta receptors and facilitating TGF-beta-induced signaling [38].
  • A TGF-beta1 monoclonal antibody, a CD40 monoclonal antibody, or a serine protease inhibitor reversed the effect of PMN CS on DC allostimulatory ability [39].
  • Lithium chloride, a GSK-3 inhibitor, increased expression of beta-catenin and attenuated TGF-beta1-dependent Smad3 signaling [40].

Physical interactions of TGFB1


Enzymatic interactions of TGFB1

  • Members of the SMAD family of intracellular proteins are phosphorylated by TGF-beta receptors and convey signals to specific TGF-beta-inducible genes [46].
  • Both Smad2 and Smad3 were phosphorylated in response to TGF-beta1 beginning at 5 minutes, with maximal phosphorylation at 15 minutes, and decreasing phosphorylation by 2 hours [47].
  • Smad2 was phosphorylated upon TGF-beta1 treatment, both in the absence and presence of genistein [48].
  • Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production [49].
  • Both wild-type TGF-beta RI and a kinase-deficient mutant thereof are transphosphorylated by the coexpressed TGF-beta RII kinase in a ligand-independent fashion in these cells [50].

Co-localisations of TGFB1


Regulatory relationships of TGFB1

  • Thus, SnoN maintains the repressed state of TGF-beta-responsive genes in the absence of ligand and participates in negative feedback regulation of TGF-beta signaling [52].
  • Using an in vitro assay, 84-100% of the TGF-beta activity could be blocked with specific antibodies against TGF-beta 2, whereas only 10-21% could be blocked by specific antibodies against TGF-beta 1 [53].
  • Akt interacts directly with Smad3 to regulate the sensitivity to TGF-beta induced apoptosis [54].
  • TGF-beta is a ubiquitously expressed cytokine that signals through the Smad proteins to regulate many diverse cellular processes [55].
  • We investigated the effects of TGF-beta 1 on the expression of tumoricidal activity induced by IL-2 or interferon-gamma (IFN-gamma) in human monocytes [56].
  • We have reported novel TRI-interacting proteins and have shown that Epac1 inhibited TGFbeta-dependent regulation of cell migration and adhesion [57].
  • IL-13 enhanced TGF-beta1-induced Smad-2 and Smad-3 phosphorylation, transient transfection with dominant-negative Smad-2 or Smad-3 decreased TIMP-1 mRNA expression in the presence of TGF-beta1 and IL-13+TGF-beta1 through inhibition of Smad-2 or Smad-3 phosphorylation [58].
  • Our experiments indicate that TGF-beta induces ET-1 expression preferentially through the ALK5/Smad3 pathway [59].
  • AMPK did not reduce TGFbeta-stimulated Smad3 COOH-terminal phosphorylation and nuclear translocation, which are necessary for MFT [60].
  • In human Burkitt lymphoma cells transformed by deregulated c-MYC expression, we demonstrate that efficient TGF-beta-induced cytostasis can occur despite both maintenance of c-MYC levels and a lack of p21 and p15 induction [61].
  • TGFbeta specifically induced the expression of Runx1 protein from an internal ribosome entry site (IRES)-dependent, cap-independent, mRNA transcript, and its overexpression was sufficient to induce hepatocyte apo pto sis [62].

Other interactions of TGFB1

  • Smad2 and Smad4 are related tumour-suppressor proteins, which, when stimulated by the growth factor TGF-beta, form a complex to inhibit growth [63].
  • Smad proteins mediate transforming growth factor-beta (TGF-beta) signaling to regulate cell growth and differentiation [52].
  • Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein [52].
  • Smad3 transactivation and TGF-beta-induced transcription were inhibited by expressing E1A, which interferes with CBP functions [64].
  • TNF-alpha, moreover, induced a high degree of resistance to the inhibitory effects of TGF-beta in a dose-dependent way [65].

Analytical, diagnostic and therapeutic context of TGFB1

  • METHODS: Using amplification refractory mutation screening PCR, we examined TGFB1 and IL10 gene polymorphisms, which are known to affect cytokine production, in 68 children with moderately severe AD and in 50 nonatopic children [66].
  • Transforming growth factor beta-1 (TGFB1)-induced gene expression was studied in five pancreatic carcinoma cell lines and one known TGFB1-sensitive cell line (HaCaT) by use of high-density filter-based cDNA microarrays representing over 4,000 human genes [29].
  • To test this hypothesis, we genotyped C-509T and Leu10Pro polymorphisms in TGFB1 and G-875A variant in TGFBR2, using the primer-introduced restriction analysis (PIRA)-PCR assay, in a case-control study of 675 gastric cancer cases and 704 healthy controls in a Chinese population [3].
  • Mutations in human BIGH3 (TGFB1), a gene identified after treatment of an adenocarcinoma cell line with TGF-beta, have been observed in patients with granular Groenouw type I, Reis-Bücklers, Thiel-Behnke, Avellino, and Lattice type I and IIIa, six autosomal dominant corneal dystrophies linked to chromosome 5q [67].
  • TGFB1 polymorphisms are associated with risk of late normal tissue complications in the breast after radiotherapy for early breast cancer [68].


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  2. Combined genetic assessment of transforming growth factor-beta signaling pathway variants may predict breast cancer risk. Kaklamani, V.G., Baddi, L., Liu, J., Rosman, D., Phukan, S., Bradley, C., Hegarty, C., McDaniel, B., Rademaker, A., Oddoux, C., Ostrer, H., Michel, L.S., Huang, H., Chen, Y., Ahsan, H., Offit, K., Pasche, B. Cancer Res. (2005) [Pubmed]
  3. Variant alleles of TGFB1 and TGFBR2 are associated with a decreased risk of gastric cancer in a Chinese population. Jin, G., Wang, L., Chen, W., Hu, Z., Zhou, Y., Tan, Y., Wang, J., Hua, Z., Ding, W., Shen, J., Zhang, Z., Wang, X., Xu, Y., Shen, H. Int. J. Cancer (2007) [Pubmed]
  4. Sp1 is required for transforming growth factor-beta-induced mesenchymal transition and migration in pancreatic cancer cells. Jungert, K., Buck, A., von Wichert, G., Adler, G., König, A., Buchholz, M., Gress, T.M., Ellenrieder, V. Cancer Res. (2007) [Pubmed]
  5. TGF-beta 1 variants in chronic beryllium disease and sarcoidosis. Jonth, A.C., Silveira, L., Fingerlin, T.E., Sato, H., Luby, J.C., Welsh, K.I., Rose, C.S., Newman, L.S., du Bois, R.M., Maier, L.A. J. Immunol. (2007) [Pubmed]
  6. TGF-beta1: a novel target for cardiovascular pharmacology. Redondo, S., Santos-Gallego, C.G., Tejerina, T. Cytokine Growth Factor Rev. (2007) [Pubmed]
  7. Inhibition of TGF-beta with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression. Biswas, S., Guix, M., Rinehart, C., Dugger, T.C., Chytil, A., Moses, H.L., Freeman, M.L., Arteaga, C.L. J. Clin. Invest. (2007) [Pubmed]
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  11. Hyaluronan orchestrates transforming growth factor-beta1-dependent maintenance of myofibroblast phenotype. Webber, J., Meran, S., Steadman, R., Phillips, A. J. Biol. Chem. (2009) [Pubmed]
  12. Association studies of transforming growth factor-beta 1 and Alzheimer's disease. Dickson, M.R., Perry, R.T., Wiener, H., Go, R.C. Am. J. Med. Genet. B Neuropsychiatr. Genet. (2005) [Pubmed]
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  26. Inhibitors of clathrin-dependent endocytosis enhance TGFbeta signaling and responses. Chen, C.L., Hou, W.H., Liu, I.H., Hsiao, G., Huang, S.S., Huang, J.S. J. Cell. Sci. (2009) [Pubmed]
  27. A mutation affecting the latency-associated peptide of TGFbeta1 in Camurati-Engelmann disease enhances osteoclast formation in vitro. McGowan, N.W., MacPherson, H., Janssens, K., Van Hul, W., Frith, J.C., Fraser, W.D., Ralston, S.H., Helfrich, M.H. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
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  29. Pancreatic carcinoma cell lines with SMAD4 inactivation show distinct expression responses to TGFB1. Jonson, T., Heidenblad, M., Håkansson, P., Gorunova, L., Johansson, B., Fioretos, T., Höglund, M. Genes Chromosomes Cancer (2003) [Pubmed]
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  31. Evidence that osteogenic progenitor cells in the human tunica albuginea may originate from stem cells: implications for peyronie disease. Vernet, D., Nolazco, G., Cantini, L., Magee, T.R., Qian, A., Rajfer, J., Gonzalez-Cadavid, N.F. Biol. Reprod. (2005) [Pubmed]
  32. Transforming growth factor B1 stimulated DNA synthesis in the granulosa cells of preantral follicles: negative interaction with epidermal growth factor. Yang, P., Roy, S.K. Biol. Reprod. (2006) [Pubmed]
  33. Histopathological and cellular studies of a case of cutaneous radiation syndrome after accidental chronic exposure to a cesium source. Vozenin-Brotons, M.C., Gault, N., Sivan, V., Tricaud, Y., Dubray, B., Clough, K., Cosset, J.M., Lefaix, J.L., Martin, M. Radiat. Res. (1999) [Pubmed]
  34. High glucose and homocysteine synergistically affect the metalloproteinases-tissue inhibitors of metalloproteinases pattern, but not TGFB expression, in human fibroblasts. Solini, A., Santini, E., Nannipieri, M., Ferrannini, E. Diabetologia (2006) [Pubmed]
  35. Expression cloning of the TGF-beta type II receptor, a functional transmembrane serine/threonine kinase. Lin, H.Y., Wang, X.F., Ng-Eaton, E., Weinberg, R.A., Lodish, H.F. Cell (1992) [Pubmed]
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  37. Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF. Fadok, V.A., Bratton, D.L., Konowal, A., Freed, P.W., Westcott, J.Y., Henson, P.M. J. Clin. Invest. (1998) [Pubmed]
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  39. Neutrophil elastase converts human immature dendritic cells into transforming growth factor-beta1-secreting cells and reduces allostimulatory ability. Maffia, P.C., Zittermann, S.E., Scimone, M.L., Tateosian, N., Amiano, N., Guerrieri, D., Lutzky, V., Rosso, D., Romeo, H.E., Garcia, V.E., Issekutz, A.C., Chuluyan, H.E. Am. J. Pathol. (2007) [Pubmed]
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