Bibliografie tematiche / TGF-beta

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Letteratura scientifica selezionata sul tema "TGF-beta"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 9 giugno 2025

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Articoli di riviste sul tema "TGF-beta"

1

Parekh, T., B. Saxena, J. Reibman, B. N. Cronstein, and L. I. Gold. "Neutrophil chemotaxis in response to TGF-beta isoforms (TGF-beta 1, TGF-beta 2, TGF-beta 3) is mediated by fibronectin." Journal of Immunology 152, no. 5 (March 1, 1994): 2456–66. http://dx.doi.org/10.4049/jimmunol.152.5.2456.

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Abstract (sommario):
Abstract TGF-beta isoforms regulate numerous cellular functions including cell growth and differentiation, the cellular synthesis and secretion of extracellular matrix proteins, such as fibronectin (Fn), and the immune response. We have previously shown that TGF-beta 1 is the most potent chemoattractant described for human peripheral blood neutrophils (PMNs), suggesting that TGF-beta s may play a role in the recruitment of PMNs during the initial phase of the inflammatory response. In our current studies, we demonstrate that the maximal chemotactic response was attained near 40 fM for all mammalian TGF-beta isoforms. However, there was a statistically significant difference in migratory distance of the PMNs: TGF-beta 2 (556 microM) > TGF-beta 3 (463 microM) > TGF-beta 1 (380 microM) (beta 2: beta 3, p < or = 0.010; beta 3: beta 1, p < or = 0.04; beta 2: beta 1, p < or = 0.0012). A mAb to the cell binding domain (CBD) of Fn inhibited the chemotactic response to TGF-beta 1 and TGF-beta 3 by 63% and to TGF-beta 2 by 70%, whereas the response to FMLP, a classic chemoattractant, was only inhibited by 18%. In contrast, a mAb to a C-terminal epitope of Fn did not retard migration (< 1.5%). The Arg-gly-Asp-ser tetrapeptide inhibited chemotaxis by approximately the same extent as the anti-CBD (52 to 83%). Furthermore, a mAb against the VLA-5 integrin (VLA-5; Fn receptor) also inhibited TGF-beta-induced chemotaxis. These results indicate that chemotaxis of PMNs in response to TGF-beta isoforms is mediated by the interaction of the Arg-gly-Asp-ser sequence in the CBD of Fn with an integrin on the PMN cell surface, primarily the VLA-5 integrin. TGF-beta isoforms also elicited the release of cellular Fn from PMNs; we observed a 2.3-fold increase in Fn (389 to 401 ng/ml) in the supernatants of TGF-beta-stimulated PMNs compared with unstimulated cells (173.6 ng/ml). The concentration of TGF-beta required to cause maximal release of Fn from PMNs (4000 fM) is a concentration at which TGF-beta is no longer chemotactic, suggesting that PMNs only use Fn that is constitutively expressed for migration. At higher concentrations of TGF-beta, the Fn released may accumulate basal to the cell, ultimately retarding cellular migration and modulating the chemotactic response.
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2

Bascom, C. C., J. R. Wolfshohl, R. J. Coffey, L. Madisen, N. R. Webb, A. R. Purchio, R. Derynck, and H. L. Moses. "Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2." Molecular and Cellular Biology 9, no. 12 (December 1989): 5508–15. http://dx.doi.org/10.1128/mcb.9.12.5508-5515.1989.

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Abstract (sommario):
Regulation of transforming growth factor beta 1 (TGF beta 1), TGF beta 2, and TGF beta 3 mRNAs in murine fibroblasts and keratinocytes by TGF beta 1 and TGF beta 2 was studied. In quiescent AKR-2B fibroblasts, in which TGF beta induces delayed stimulation of DNA synthesis, TGF beta 1 autoregulation of TGF beta 1 expression was observed as early as 1 h, with maximal induction (25-fold) after 6 to 12 h. Increased expression of TGF beta 1 mRNA was accompanied by increased TGF beta protein production into conditioned medium of AKR-2B cells. Neither TGF beta 2 nor TGF beta 3 mRNA, however, was significantly induced, but both were apparently down regulated at later times by TGF beta 1. Protein synthesis was not required for autoinduction of TGF beta 1 mRNA in AKR-2B cells. Nuclear run-on analyses and dactinomycin experiments indicated that autoregulation of TGF beta 1 expression is complex, involving both increased transcription and message stabilization. In contrast to TGF beta 1, TGF beta 2 treatment of quiescent AKR-2B cells increased expression of TGF beta 1, TGF beta 2, and TGF beta 3 mRNAs, but with different kinetics. Autoinduction of TGF beta 2 mRNA occurred rapidly with maximal induction at 1 to 3 h, enhanced TGF beta 3 mRNA levels were observed after 3 h, and increased expression of TGF beta 1 occurred later, with maximal mRNA levels obtained after 12 to 24 h. Nuclear run-on analyses indicated that TGF beta 2 regulation of TGF beta 2 and TGF beta 3 mRNA levels is transcriptional, while TGF beta 2 induction of TGF beta 1 expression most likely involves both transcriptional and posttranscriptional controls. In BALB/MK mouse keratinocytes, minimal autoinduction of TGF beta 1 occurred at only the 12- and 24-h time points and protein synthesis was required for this autoinduction. The results of this study provide an example in which TGF beta 1 and TGF beta 2 elicit different responses and demonstrate that expression of TGF beta 1, and TGF beta 3 are regulated differently. The physiological relevance of TGF beta 1 autoinduction in the context of wound healing is discussed.
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3

Bascom, C. C., J. R. Wolfshohl, R. J. Coffey, L. Madisen, N. R. Webb, A. R. Purchio, R. Derynck, and H. L. Moses. "Complex regulation of transforming growth factor beta 1, beta 2, and beta 3 mRNA expression in mouse fibroblasts and keratinocytes by transforming growth factors beta 1 and beta 2." Molecular and Cellular Biology 9, no. 12 (December 1989): 5508–15. http://dx.doi.org/10.1128/mcb.9.12.5508.

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Abstract (sommario):
Regulation of transforming growth factor beta 1 (TGF beta 1), TGF beta 2, and TGF beta 3 mRNAs in murine fibroblasts and keratinocytes by TGF beta 1 and TGF beta 2 was studied. In quiescent AKR-2B fibroblasts, in which TGF beta induces delayed stimulation of DNA synthesis, TGF beta 1 autoregulation of TGF beta 1 expression was observed as early as 1 h, with maximal induction (25-fold) after 6 to 12 h. Increased expression of TGF beta 1 mRNA was accompanied by increased TGF beta protein production into conditioned medium of AKR-2B cells. Neither TGF beta 2 nor TGF beta 3 mRNA, however, was significantly induced, but both were apparently down regulated at later times by TGF beta 1. Protein synthesis was not required for autoinduction of TGF beta 1 mRNA in AKR-2B cells. Nuclear run-on analyses and dactinomycin experiments indicated that autoregulation of TGF beta 1 expression is complex, involving both increased transcription and message stabilization. In contrast to TGF beta 1, TGF beta 2 treatment of quiescent AKR-2B cells increased expression of TGF beta 1, TGF beta 2, and TGF beta 3 mRNAs, but with different kinetics. Autoinduction of TGF beta 2 mRNA occurred rapidly with maximal induction at 1 to 3 h, enhanced TGF beta 3 mRNA levels were observed after 3 h, and increased expression of TGF beta 1 occurred later, with maximal mRNA levels obtained after 12 to 24 h. Nuclear run-on analyses indicated that TGF beta 2 regulation of TGF beta 2 and TGF beta 3 mRNA levels is transcriptional, while TGF beta 2 induction of TGF beta 1 expression most likely involves both transcriptional and posttranscriptional controls. In BALB/MK mouse keratinocytes, minimal autoinduction of TGF beta 1 occurred at only the 12- and 24-h time points and protein synthesis was required for this autoinduction. The results of this study provide an example in which TGF beta 1 and TGF beta 2 elicit different responses and demonstrate that expression of TGF beta 1, and TGF beta 3 are regulated differently. The physiological relevance of TGF beta 1 autoinduction in the context of wound healing is discussed.
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4

ten Dijke, P., K. K. Iwata, C. Goddard, C. Pieler, E. Canalis, T. L. McCarthy, and M. Centrella. "Recombinant transforming growth factor type beta 3: biological activities and receptor-binding properties in isolated bone cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4473–79. http://dx.doi.org/10.1128/mcb.10.9.4473-4479.1990.

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Abstract (sommario):
We have recently cloned the cDNA for transforming growth factor type beta 3 (TGF-beta 3), a new member of the TGF-beta gene family. We examined the biological effects of recombinant TGF-beta 3 protein in osteoblast-enriched bone cell cultures. In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity. In a direct comparison between TGF-beta 3 and TGF-beta 1, TGF-beta 3 appeared to be three- to fivefold more potent than TGF-beta 1. Our cross-linking experiments with iodinated TGF-beta showed that in osteoblast-enriched bone cell cultures, both TGF-beta 3 and TGF-beta 1 associated with the same three cell surface binding sites. Scatchard analysis of receptor competition studies indicated the presence of high-affinity binding sites for TGF-beta 3 in the picomolar range. TGF-beta 3 showed an approximately fourfold-higher apparent affinity than TGF-beta 1 in overall binding.
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ten Dijke, P., K. K. Iwata, C. Goddard, C. Pieler, E. Canalis, T. L. McCarthy, and M. Centrella. "Recombinant transforming growth factor type beta 3: biological activities and receptor-binding properties in isolated bone cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4473–79. http://dx.doi.org/10.1128/mcb.10.9.4473.

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Abstract (sommario):
We have recently cloned the cDNA for transforming growth factor type beta 3 (TGF-beta 3), a new member of the TGF-beta gene family. We examined the biological effects of recombinant TGF-beta 3 protein in osteoblast-enriched bone cell cultures. In this report we demonstrate that TGF-beta 3 is a potent regulator of functions associated with bone formation, i.e., mitogenesis, collagen synthesis, and alkaline phosphatase activity. In a direct comparison between TGF-beta 3 and TGF-beta 1, TGF-beta 3 appeared to be three- to fivefold more potent than TGF-beta 1. Our cross-linking experiments with iodinated TGF-beta showed that in osteoblast-enriched bone cell cultures, both TGF-beta 3 and TGF-beta 1 associated with the same three cell surface binding sites. Scatchard analysis of receptor competition studies indicated the presence of high-affinity binding sites for TGF-beta 3 in the picomolar range. TGF-beta 3 showed an approximately fourfold-higher apparent affinity than TGF-beta 1 in overall binding.
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6

Nunes, I., R. L. Shapiro, and D. B. Rifkin. "Characterization of latent TGF-beta activation by murine peritoneal macrophages." Journal of Immunology 155, no. 3 (August 1, 1995): 1450–59. http://dx.doi.org/10.4049/jimmunol.155.3.1450.

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Abstract (sommario):
Abstract Transforming growth factor-beta (TGF-beta) is secreted by most cells as a biologically inactive complex, called the large latent TGF-beta complex. The complex is comprised of latent TGF-beta binding protein (LTBP) and latent TGF-beta, which is mature TGF-beta associated noncovalently with its amino-terminal propeptides. LTBP is disulfide-linked to the amino-terminal propeptide of latent TGF-beta. Active TGF-beta is generated by release of TGF-beta from the complex. Generation of active TGF-beta by macrophages has been reported, but the activation mechanism has not been described. Latent TGF-beta activation by macrophages was characterized using serum-free cultures of resident and thioglycollate-elicited murine peritoneal macrophages that were either unstimulated or LPS-stimulated in vitro. Serum-free conditioned medium was assayed for TGF-beta using a quantitative luciferase-based bioassay. LPS-stimulated thioglycollate-elicited macrophages activated endogenous latent TGF-beta, whereas non-LPS-stimulated thioglycollate-elicited and resident macrophages generated undetectable levels of TGF-beta. Latent TGF-beta activation required plasmin and urokinase (uPA), uPA binding to the uPA receptor, interaction with the cation-independent mannose 6-phosphate/insulin-like growth factor type II receptor, tissue type II transglutaminase, and LTBP. A time-course analysis of latent TGF-beta activation revealed that maximal TGF-beta was generated after 24 h (25 +/- 5 pg/ml). TGF-beta formed within the initial 24 h modulated the plasminogen activator system by down-regulating uPA, suggesting that TGF-beta temporally modulated its own formation by regulating cell-associated uPA.
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7

Villiger, P. M., A. B. Kusari, P. ten Dijke, and M. Lotz. "IL-1 beta and IL-6 selectively induce transforming growth factor-beta isoforms in human articular chondrocytes." Journal of Immunology 151, no. 6 (September 15, 1993): 3337–44. http://dx.doi.org/10.4049/jimmunol.151.6.3337.

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Abstract (sommario):
Abstract Transforming growth factor-beta (TGF-beta) plays an important role in homeostasis of connective tissues, but regulation of its expression in mesenchymal cells is not well characterized. This study examines the effects of the cytokines IL-1 beta and IL-6 on expression of TGF-beta isoforms in human articular chondrocytes. IL-6 caused a fivefold increase, in the secretion of TGF-beta bioactivity by primary chondrocytes, whereas IL-1 beta showed only marginal stimulatory effects. Analysis by Northern blotting showed that IL-6 induced TGF-beta 1 gene expression but had no detectable effect on TGF-beta 2 mRNA levels and marginally increased TGF-beta 3 mRNA. However, IL-1 inhibited TGF-beta 1 mRNA expression induced by serum. In contrast, IL-1 beta strongly and selectively upregulated the TGF-beta 3 isoform. To determine whether this differential effect of IL-1 beta resulted in a corresponding change in protein synthesis, chondrocytes were metabolically labeled and analyzed by immunoprecipitation. IL-1 beta selectively induced TGF-beta 3 protein synthesis but reduced synthesis of the TGF-beta 1 and TGF-beta 2 isoforms. Consistent with the effects on TGF-beta 1 mRNA, IL-6 increased the synthesis of TGF-beta 1. These differential effects of the cytokines IL-1 beta and IL-6 provide new insight into the regulation of TGF-beta expression and may represent a protective mechanism against cytokine-induced connective tissue catabolism.
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8

Siepl, C., U. V. Malipiero, and A. Fontana. "Transforming growth factor-beta (TGF-beta)-resistant helper T lymphocyte clones show a concomitant loss of all three types of TGF-beta receptors." Journal of Immunology 146, no. 9 (May 1, 1991): 3063–67. http://dx.doi.org/10.4049/jimmunol.146.9.3063.

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Abstract (sommario):
Abstract Three ovalbumin-specific T helper cell lines (OVA-7T cells) that differ in their susceptibility to the immunosuppressive effects of transforming growth factor-beta (TGF-beta) were cloned. The frequency of TGF-beta-resistant OVA-7T cell clones correlated with the decline of TGF-beta sensitivity in the original OVA-7T parental cell lines. In TGF-beta-resistant OVA-7T cell clones, TGF-beta inhibited neither the growth of the T cells nor their secretion of granulocyte macrophage CSF. TGF-beta suppressed the expression of c-myc mRNA in OVA-7T-responder but not in OVA-7T-nonresponder cells. TGF-beta resistance was found to be due to a loss of TGF-beta high-affinity binding sites, with an absence of expression of the distinct 54-, 70-, 110-, and 250-kDa surface proteins that bind TGF-beta on TGF-beta-susceptible T cells. Loss of TGF-beta R may enable T cells to escape the negative feedback control provided by TGF-beta secreted from activated T cells during an immune response.
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9

Pelton, R. W., B. Saxena, M. Jones, H. L. Moses, and L. I. Gold. "Immunohistochemical localization of TGF beta 1, TGF beta 2, and TGF beta 3 in the mouse embryo: expression patterns suggest multiple roles during embryonic development." Journal of Cell Biology 115, no. 4 (November 15, 1991): 1091–105. http://dx.doi.org/10.1083/jcb.115.4.1091.

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Abstract (sommario):
Isoform-specific antibodies to TGF beta 1, TGF beta 2, and TGF beta 3 proteins were generated and have been used to examine the expression of these factors in the developing mouse embryo from 12.5-18.5 d post coitum (d.p.c.). These studies demonstrate the initial characterization of both TGF beta 2 and beta 3 in mammalian embryogenesis and are compared with TGF beta 1. Expression of one or all three TGF beta proteins was observed in many tissues, e.g., cartilage, bone, teeth, muscle, heart, blood vessels, lung, kidney, gut, liver, eye, ear, skin, and nervous tissue. Furthermore, all three TGF beta proteins demonstrated discrete cell-specific patterns of expression at various stages of development and the wide variety of tissues expressing TGF beta proteins represent all three primary embryonic germ layers. For example, specific localization of TGF beta 1 was observed in the lens fibers of the eye (ectoderm), TGF beta 2 in the cortex of the adrenal gland (mesoderm), and TGF beta 3 in the cochlear epithelium of the inner ear (endoderm). Compared to the expression of TGF beta mRNA transcripts in a given embryonic tissue, TGF beta proteins were frequently colocalized within the same cell type as the mRNA, but in some cases were observed to localize to different cells than the mRNA, thereby indicating that a complex pattern of transcription, translation, and secretion for TGF beta s 1-3 exists in the mouse embryo. This also indicates that TGF beta 1, beta 2, and beta 3 act through both paracrine and autocrine mechanisms during mammalian embryogenesis.
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10

Waltenberger, J., A. Wanders, B. Fellström, K. Miyazono, C. H. Heldin, and K. Funa. "Induction of transforming growth factor-beta during cardiac allograft rejection." Journal of Immunology 151, no. 2 (July 15, 1993): 1147–57. http://dx.doi.org/10.4049/jimmunol.151.2.1147.

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Abstract (sommario):
Abstract The polypeptides of the transforming growth factor-beta (TGF-beta) family are potent endogenous immuno-regulators. Using a rat cardiac allograft transplant model, we investigated the expression of the precursor forms of TGF-beta 1, TGF-beta 2, and TGF-beta 3 and the latent TGF-beta binding protein (LTBP) by immunohistochemistry. The activity of TGF-beta in the extracts from transplanted as well as normal hearts was measured using a bioassay, and Northern blot analysis was performed on RNA extracts. The transplanted hearts were analyzed both during acute rejection up to 6 days and during chronic rejection up to 6 mo after transplantation and compared with normal controls. The animals of the chronic rejection group received cyclosporin A for immunosuppression. The TGF-beta bioactivity dramatically increased in the transplanted allografts during the chronic rejection process compared to the normal hearts, and so did the immunostaining as well as the mRNA levels for TGF-beta 1 and, to a lesser extent, the immunostaining for TGF-beta 2. TGF-beta 3 expression remained unchanged and was only found in the myocardium in trace amounts. During the acute rejection process up to 6 days after transplantation, TGF-beta immunoreactivity increased only slightly, whereas the TGF-beta mRNA was severalfold increased. Control animals treated with cyclosporin A showed a similar pattern at day 6 with regard to TGF-beta expression. LTBP was induced simultaneously with TGF-beta 1 and occurred within interstitial spaces of the myocardium. The TGF-beta was produced by macrophage-like infiltrating lymphocytes. In conclusion, highly elevated levels of TGF-beta and LTBP were found during chronic rejection of cardiac allografts in rats. The induction of TGF-beta may counteract the rejection process and could be useful for new therapeutic approaches in the prevention of allograft rejection.
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Tesi sul tema "TGF-beta"

1

Bünemann, Christoph Lars. "Molekulare Mechanismen der Inhibition TGF-[beta]-induzierter [TGF-beta-induzierter] Apoptose in Hepatomzellen." [S.l. : s.n.], 2000. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8560503.

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Ouyang, Nengtai. "Effects of TGF-[beta]1 [TGF-beta-1] in ischemia, reperfusion injury and chronic allograft nephropathy." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972198628.

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Köhler, Heike Christine. "Die TGF-[beta] [TGF-beta] vermittelte Suppression der antigenspezifischen Immunantwort kann durch CD28 Kostimulation überwunden werden." München Verl. Dr. Hut, 2008. http://d-nb.info/992163080/04.

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Mecha, Ezekiel Onyonka [Verfasser]. "Characterization of the TGF-beta signalosome and of TGF-beta-dependent endometrial cell proliferation / Ezekiel Onyonka Mecha." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/1068590459/34.

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Choi, Won Seon 1975. "Involvement of TGF-beta in skin photoaging." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33842.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2005.<br>Vita.<br>Includes bibliographical references.<br>The goal of this thesis study was to understand the role of TGF-[beta] in skin photoaging, especially in solar elastosis. Solar elastosis, the accumulation of elastotic material in the dermal extracelluar matrix, is a major hallmark of photoaging. However, the mechanisms by which UV radiation causes solar elastosis are poorly understood. TGF-[beta] is a multifunctional cytokine involved in the regulation of extracelluar matrix and is known to be up-regulated by UVR. Involvement of reactive oxygen species (ROS) in the development of solar elastosis has been demonstrated by many studies using antioxidants and anti-inflammatory agents in the mouse skin in vivo. We hypothesized that ROS produced by TGF-[beta] are key components in the tropoelastin (TE, a soluble precursor of elastin) up-regulation in dermal fibroblasts, and that TGF-[beta] is a major regulator in the photoaging processes. Using human skin fibroblasts system in vitro, we found that ROS generated from NADPH oxidase and mitochondria are involved in the TGF-[beta] induced elastin production, and intracellular sources of ROS vary with time. We showed that both Smad and non-Smad pathways, e.g. MAPK and PKC pathways, are required for TE mRNA up-regulation by TGF-[beta].<br>(cont.) However, ROS were not involved in some of the important steps in these pathways, such as phosphorylations of p38 or ERK or Smad2, suggesting that ROS acts downstream of these pathways. The in vivo chronic UVB irradiation study using a Skh- 1 hairless mouse model with a small molecule inhibitor for the TGF-[beta] type I receptor showed that the TGF-[beta] receptor inhibitor increased the number of mast cells, but decreased the levels of active TGF-[beta] protein, and mRNA levels for collagen III and IV, MMP-2 and 9, and TE in the chronically UVB irradiated mouse skin. However, those responses did not result in the changes in the collagen and elastin content, or the wrinkle formation. Overall, this work indicates that TGF-[beta] contributes to the solar elastosis, through the effects on the TE mRNA level in skin. Implication of this role of TGF-[beta] in the elastin fiber deposition or visible changes of photoaged skin requires further investigation.<br>by Won Seon Choi.<br>Ph.D.
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Dudu, Veronica. "TGF-beta signaling at the cellular junctions." [S.l. : s.n.], 2005. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11878497.

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Peri, Francesca. "The role of EGF and TGF-[beta] [TGF-beta] signaling specifying the polarity of the Drosophila egg and embryo." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963638386.

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Kroner, Antje. "Klonierung und Charakterisierung von Rezeptorkinasen der EGF- und TGF[beta]-Familie [TGF-Beta-Familie] des kleinen Fuchsbandwurmes Echinococcus multilocularis." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969749481.

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Möller, Antje. "Proliferation von Lungenfibroblasten in vitro unter dem Einfluss von ionisierender Strahlung bzw. von TGF-[beta]1 [TGF-beta-1]." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=974672165.

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10

Serwe, Annegret. "Hemmung der Angiogenese und Tumorprogression durch Blockierung der TGF-[beta]-Signaltransduktion [TGF-Beta-Signaltransduktion] durch neue Wirkstoffe isoliert aus Pilzen." Duisburg Köln WiKu, 2007. http://d-nb.info/987489674/04.

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Libri sul tema "TGF-beta"

1

Zi, Zhike, and Xuedong Liu, eds. TGF-Beta Signaling. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2277-3.

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2

Benson, John R. TGF [beta] and cancer. Austin: R.G. Landes, 1998.

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3

Rik, Derynck, and Miyazono Kōhei 1956-, eds. The TGF-[beta] family. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2008.

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4

Gregory, Bock, Marsh Joan, and Symposium on Clinical Applications of TGF-[beta] (1990 : Ciba Foundation), eds. Clinical applications of TGF-[beta]. Chichester: Wiley, 1991.

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5

Winter, Jennifer Leslie. Oxygen regulation of TGF[beta]3 expression in the human placenta. Ottawa: National Library of Canada, 2001.

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6

Müller, Gesine Frauke. Interaktion zwischen "aryl hydrocarbon receptor" (AhR) und 'transforming growth factor-[beta]₁' (TGF-[beta]₁): Speziesspezifität und Zellzykluskontrolle. Hannover: [s.n.], 1999.

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7

Chiang, Theodore Andrew. SARA is a novel anchoring protein essential for TGF-[beta] signal transduction. Ottawa: National Library of Canada, 1998.

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8

Davison, Anne Frances. Characterization of the Smad anchor for receptor activation in TGF[beta] signal transduction. Ottawa: National Library of Canada, 2000.

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Copland, Ian. Correlation of changes in morphology and TGF-[beta] expression during human umbilical cord development. Ottawa: National Library of Canada, 2000.

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Cruz, Briolange Maria. Transforming growth factor beta (TGF-[beta]) regulates macrophage procoagulant activity (PCA) induction by murine hepatitis virus strain 3 (MHV-3). Ottawa: National Library of Canada, 1994.

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Capitoli di libri sul tema "TGF-beta"

1

Teicher, Beverly. "TGF Beta Receptors." In Cancer Therapeutic Targets, 479–85. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_75.

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Teicher, Beverly. "TGF Beta Receptors." In Cancer Therapeutic Targets, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6613-0_75-2.

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Huber, Samuel, Enric Esplugues, and Richard A. Flavell. "TGF-beta and TH17 Cells." In TH17 Cells in Health and Disease, 41–45. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7_3.

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Dennler, Sylviane, and Peter Ten Dijke. "Smad Proteins in TGF-Beta Signaling." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_5364-2.

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Wan, Yisong Y., and Richard A. Flavell. "TGF-Beta and Regulatory T Cells." In Regulatory T Cells and Clinical Application, 91–109. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-77909-6_6.

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Dennler, Sylviane, and Peter ten Dijke. "Smad Proteins in TGF-Beta Signaling." In Encyclopedia of Cancer, 4257–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_5364.

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Dennler, Sylviane, and Peter Ten Dijke. "Smad Proteins in TGF-Beta Signaling." In Encyclopedia of Cancer, 3440–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5364.

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Gaedeke, J., H. Peters, N. A. Noble, and W. A. Border. "Angiotensin II, TGF-β and Renal Fibrosis." In Contributions to Nephrology, 153–60. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000060162.

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Chen, W., and S. M. Wahl. "TGF-β: Receptors, Signaling Pathways and Autoimmunity." In Current Directions in Autoimmunity, 62–91. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000060548.

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Fabregat, Isabel, та Patricia Sancho. "The Transforming Growth Factor-Beta (TGF-β) in Liver Fibrosis". У TGF-β in Human Disease, 255–77. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54409-8_11.

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Atti di convegni sul tema "TGF-beta"

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Hanson, Josiah F., and Gustavo Matute-Bello. "Fas-Induced Lung Injury Requires TGF-Beta Activity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4010.

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Winter, P., T. Wartmann, K. Hippe, L. Wilkens, R. Croner, and U. Kahlert. "TGF-beta Pseudorezeptor BAMBI als Therapieziel im Pankreastumor." In Viszeralmedizin 2024. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1789932.

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Dropmann, A., S. Dooley, B. Dewidar, S. Ghafoori, S. Woelfl, S. Hammad, V. Nalewaja, et al. "TGF-beta 2 als therapeutische Zielstruktur bei cholestatischer Leberfibrose." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695252.

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Seoane, Joan. "Abstract CN06-02: TGF-beta and cancer stem cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-cn06-02.

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Zheng, Yanbin, Patricia Chu, and Stephen X. Skapek. "Abstract 1140: C/ebp beta repressesArfinduction by tgf-beta2." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1140.

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Khan, I. S., T. Tsukui, X. Ren, and D. Sheppard. "TGF-Beta Signaling in Lung Development and Bronchopulmonary Dysplasia." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2528.

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Boujelbene, Nadia, Ines Zemni, Wafa Babay, Sana Baroudi, Ameni Dridi, Ines Ben Safta, Imen Ouzari, and Ines Zidi. "240 TGF-beta gene polymorphism and ovarian cancer susceptibility." In ESGO 2024 Congress Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/ijgc-2024-esgo.599.

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Zwaagstra, John, Traian Sulea, Anne E. G. Lenferink, Jason Baardsnes, Catherine Collins, Christiane Cantin, Lucie Couture, Limei Tao, Yves Durocher, and Maureen O'Connor-McCourt. "Abstract B024: Single-chain traps targeting transforming growth factor-beta (TGF-beta) home to tumors and reduce tumor growth and metastasis by counteracting TGF-beta-mediated immunosuppression." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b024.

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Tu, Kangsheng, Jiachu Li, Chunsheng Liu, Vijay H. Shah, and Ningling Kang. "Abstract A70: Vasodilator-stimulated phosphoprotein promotes TGF-beta mediated myofibroblastic activation by regulating recycling of TGF-beta receptor II to the plasma membrane." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a70.

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Mosley-Brown, Adenike, Xiaojing Li, Kenneth Poon, Karina Serban, Matthew Cable, Paul Kogut, and Blanca Camoretti-Mercado. "Localization Of TGF Beta (TGF-b) Receptors Within The Nuclei Of Human Airway Smooth Muscle Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5315.

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Rapporti di organizzazioni sul tema "TGF-beta"

1

สุทธมนัสวงษ์, สุภาพร, จีรศักดิ์ นพคุณ та ประสิทธิ์ ภวสันต์. บทบาทของ TGF-beta1 ในกระบวนการดิฟเฟอเรนชิเอชันของเซลล์เพาะเลี้ยงจากเนื้อเยื่อโพรงฟันของมนุษย์ : รายงานผลการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2000. https://doi.org/10.58837/chula.res.2000.6.

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Abstract (sommario):
TGF-[beta]1 เป็นโกร๊ทแฟคเตอร์ที่มีบทบาทอย่างมากในเมตาบอลิซึมของเซลล์กระดูกและฟัน งานวิจัยครั้งนี้มีจุดมุ่งหมายเพื่อศึกษาการตอบสนองของเซลล์เพาะเลี้ยงจากเนื้อเยื่อโพรงฟันของมนุษย์ต่อ TGF-[beta]1 ในแง่ของการเปลี่ยนแปลงของระดับเอนไซม์อัลคาไลน์ฟอสฟาเตส และระดับการแสดงออกของออสติโอแคลซิน รวมทั้งเปรียบเทียบความสัมพันธ์ของการเปลี่ยนแปลงดังกล่าวกับการเปลี่ยนแปลงระดับการแสดงออกของ BMP และ BMPR เซลล์โพรงฟันถูกกระตุ้นด้วย TGF-[beta]1 ที่ความเข้มข้น 0, 0.1, 1 และ 10 นาโนกรัม/มิลลิลิตร เป็นเวลา 3 และ 5 วัน ผลการทดลองพบว่า ระดับเอนไซม์อัลคาไลน์ฟอสฟาเตสในเซลล์กลุ่มที่ได้รับ TGF-[beta]1 ที่ความเข้มข้น 0.1 และ 1 นาโนกรัม/มิลลิลิตรจะเพิ่มสูงขึ้นกว่ากลุ่มควบคุมอย่างชัดเจนในวันที่ 5 และไม่พบความแตกต่างของออสติโอแคลซินระหว่างกลุ่มควบคุมและกลุ่มทดลองทั้งในวันที่ 3 และ 5 ระดับการแสดงออกของ BMP-2, BMP-4, BMPRI-A และ BMPR-II จะเพิ่มขึ้นในกลุ่มที่ได้รับ TGF-[beta]1 ที่ความเข้มข้น 0.1 และ 1 นาโนกรัม-มิลลิลิตรในวันที่ 5 เช่นเดียวกับเอนไซม์อัลคาไลน์ฟอสฟาเตส เมื่อทดลองกระตุ้นเซลล์ด้วย TGF-[beta]1 ที่ความเข้มข้น 0.1 และ 1 นาโนกรัม/มิลลิลิตร 2 แบบ คือแบบ 7 วัน หรือแบบที่กระตุ้นในช่วง 5 วันแรก แต่ไม่มี TGF-[beta]1 ใน 2 วันถัดมา (แบบ 5+2 วัน) ผลปรากฏว่าระดับของเอนไซม์อัลคาไลน์ฟอสฟาเตสจะเพิ่มสูงขึ้นอย่างมากในแบบ 7 วัน แต่ไม่พบการเปลี่ยนแปลงของออสติโอแคลซิน ในขณะที่ระดับเอนไซม์อัลคาไลน์ฟอสฟาเตสจะไม่เพิ่มสูงมากนักในแบบ 5+2 แต่ระดับของออสติโอแคลซินเพิ่มขึ้นถึง 2 เท่า และการแสดงออกของ BMP-2, BMP-4, BMPRI-A และ BMPR-II จะเพิ่มสูงกว่ากลุ่มควบคุมอย่างชัดเจนเฉพาะในแบบ 5+2 วันเท่านั้น โดยที่การเพิ่มขึ้นของระดับเอนไซม์อัลคาไลน์ฟอสฟาเตส และออสติโอแคลซิน แสดงถึงการเปลี่ยนแปลงระดับดิฟเฟอเรนซิเอชันของเซลล์โพรงฟัน ดังนั้นผลการทดลองนี้ แสดงว่า TGF-[beta]1 มีอิทธิพลต่อระดับดิฟเฟอเรนซิเอชันของเซลล์โพรงฟัน โดยแปรผันกับความเข้มข้น และระยะเวลาที่เซลล์สัมผัสกับ TGF-[beta]1 นอกจากนี้ การคงอยู่ในระยะยาวของ TGF-[beta]1 ก็อาจเป็นตัวแปรหนึ่งที่สำคัญต่อระดับดิฟเฟอเรนซิเอชันของเซลล์โพรงฟันด้วย และโดยที่การเปลี่ยนแปลงของระดับเอนไซม์อัลคาไลน์ฟอสฟาเตสและออกสติโอแคลซิน สอดคล้องกับการเปลี่ยนแปลงการแสดงออกของ BMP และ BMPR ดังนั้น จึงมีความเป็นไปได้ที่การแสดงออกของ BMP และ BMPR จะเกี่ยวข้องกับดิฟเฟอเรนซิเอชันของเซลล์โพรงฟันที่ถูกเหนี่ยวนำด้วย TGF-[beta]1
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สารชวนะกิจ, นีรชา, ประสิทธิ์ ภวสันต์ та อาทิพันธุ์ พิมพ์ขาวขำ. การควบคุมการแสดงออกของเอนไซม์เอ็มเอ็มพี-9 โดยทรานส์ฟอร์มมิงโกรทแฟคเตอร์เบตาในเซลล์มะเร็งช่องปากชนิดสแควมัสเซลล์ : รายงานวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2007. https://doi.org/10.58837/chula.res.2007.17.

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เอนไซม์ MMP-9 เป็นเอนไซม์ที่มีความเกี่ยวข้องกับการแพร่กระจายของเซลล์มะเร็งไปยังเนื้อเยื่อข้างเคียง TGF-[beta] เป็นโกรทเฟคเตอร์ ซึ่งเกี่ยวข้องกับกระบวนการต่างๆ ของเซลล์ เช่น การเพิ่มจำนวนเซลล์การดิฟเฟอเรนชิเอท และการตายแบบ Apoptosis เป็นต้น อย่างไรก็ตาม ในรอยโรคมะเร็งมีรายงานว่า TGF-[beta] มีผลต้านทานการแพร่กระจายของเซลล์มะเร็งระยะแรก แต่กระตุ้นการแพร่กระจายของเซลล์มะเร็งในระยะลุกลาม การทดลองครั้งนี้ ทำการศึกษาผลของ TGF-[beta] ที่มีต่อการแสดงออก และการกระตุ้นการทำงานของเอนไซม์ MMP-9 ในเซลล์ไลน์ของมะเร็งชนิดสแควมัสเซลล์ที่พบในช่องปาก และกลไกในระดับอณู ตลอดจนความสัมพันธ์ระหว่างเซลล์มะเร็งชนิดสแควมัสเซลล์ที่พบในช่องปาก กับเซลล์เนื้อเยื่อเกี่ยวพันที่ได้จากเหงือกในแง่ของการเหนี่ยวนำการเปลี่ยนแปลงระดับการสร้าง TGF-[beta] ผลการทดลองแสดงให้เห็นว่า TGF-[beta] สามารถเหนี่ยวนำให้เซลล์มะเร็งชนิดสแควมัสเซลล์ หลั่งเอนไซม์ MMP-9 เพิ่มขึ้น สัญญาณการกระตุ้นเกิดผ่าน crosstalk ระหว่างเส้นทางการส่งถ่ายสัญญาณของ Smad และ Rho kinase นอกจากนี้ เซลล์มะเร็งชนิดสแควมัสเซลล์ที่พบในช่องปาก ยังสามารถกระตุ้นเซลล์ของเนื้อเยื่อเกี่ยวพันให้หลั่ง MMP-9 เพิ่มขึ้น แต่กลไกการเหนี่ยวนำยังไม่มีความชัดเจน
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Wang, Xiao-Fan. The Roles of TGF-Beta and TGF-Beta Signaling Receptors in Breast Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada302476.

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Wang, Xiao-Fan. The Roles of TGF-Beta and TGF-Beta Signaling Receptors in Breast Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada315705.

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Dabovic, Branka B., and Daniel B. Rifkin. TGF-Beta and Breast Cancer Induction. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407399.

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Liu, Fang. TGF-Beta Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429736.

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Wieder, Robert. The Roles of FGF-2 TGF Beta and TGF Beta Receptor 2 in Breast Cancer Dormancy. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418963.

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Jobling, Michael, Mary H. Barcellos-Hoff, and Joni Mott. Bioavailability of TGF-Beta in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada444006.

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Jobling, Michael F. Bioavailability of TGF-Beta in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada429598.

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Illa-Bochaca, Irineu, and Mary H. Barcellos-Hoff. Bioavailability of TGF-Beta in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada474704.

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