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Chia, Choy May. "Epidermal growth factor (EGF) : transforming growth factor alpha (TGF-#alpha#) in human preimplantation development". Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362631.
Pełny tekst źródłaLau, Kwok-pui. "Clinicopathological roles of transforming growth factor alpha (TGF[alpha]) in papillary thyroid carcinoma /". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39558733.
Pełny tekst źródłaLam, Sze-man Joyce. "Expression of transforming growth factors (TGF-alpha and TGF-beta 1) on postmortem skin wounds /". View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38480566.
Pełny tekst źródłaLiu, Xiaoying. "Molecular mechanisms of myofibroblast differentiation and the role of TGF beta1, TNF alpha, and thrombin signal transduction". Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1236711907.
Pełny tekst źródłaGlinsmann-Gibson, Betty Jean 1961. "Molecular mechanism of autocrine regulation by TGF-alpha in T(3)M(4) human pancreatic carcinoma cells". Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277113.
Pełny tekst źródłaHallbeck, Anna-Lotta. "Studies of transforming growth factor alpha in normal and abnormal growth". Doctoral thesis, Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med1025s.pdf.
Pełny tekst źródła林詩敏 i Sze-man Joyce Lam. "Expression of transforming growth factors (TGF-alpha and TGF-beta 1) on postmortem skin wounds". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011400.
Pełny tekst źródłaKiesow, Claudia. "Pathogenese der equinen Endometrose: Bedeutung der Wachstumsfaktoren Transforming growth factor-alpha, -beta1, -beta2 und -beta3 sowie der Matrixmetalloproteinase-2". Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-65079.
Pełny tekst źródła劉國培 i Kwok-pui Lau. "Clinicopathological roles of transforming growth factor alpha (TGFα) in papillary thyroid carcinoma". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558733.
Pełny tekst źródłaFreese, Christiane. "Rolle der Plasmakonzentrationen von transforming growth factor-[beta]1 [factor-beta1] (TGF[beta]1) [TGF beta 1], Tumor necrosis factor [alpha] [Tumor necrosis factor alpha] (TNF [alpha]) [TNF alpha] und Plasminogen-Activator-Inhibitor-(PAI-)-Antigen bei Patienten mit Diabetes Mellitus Typ 2 und koronarer Herzkrankheit". [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=97149200X.
Pełny tekst źródłaMongerard-Coulanges, Medge. "Influence de l'expression du facteur de croissance VEGF sur l'activité antitumorale de l'alendronate". Paris 6, 2009. http://www.theses.fr/2009PA066596.
Pełny tekst źródłaLautrette, Alexandre. "Interaction entre la voie de l'épidermal growth factor et la voie de l'angiotensine : rôle dans la progression des lésions rénales". Paris 6, 2006. http://www.theses.fr/2006PA066376.
Pełny tekst źródłaMaltman, John. "A study of the interactions between macrophage inflammatory protein 1 alpha (MIP-1#alpha#) and transforming growth factor beta (TGF-#beta#) in the control of haemopoietic stem cell proliferation". Thesis, University of Glasgow, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301654.
Pełny tekst źródłaHerbert, Brittney-Shea. "Mechanisms of RRR-[alpha]-tocopheryl succinate- and N-(4-hydroxyphenyl)retinamide-induced apoptosis of human HL-60 myelocytic leukemia and MDA-MB-435 breast cancer cells : a role for TGF-[beta] and C-JUN /". Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
Pełny tekst źródłaPerlemuter, Gabriel. "Capside du virus de l'hépatite C et métabolisme lipidique hépatique". Paris 7, 2002. http://www.theses.fr/2002PA077147.
Pełny tekst źródłaBonniaud, Philippe. "Transforming growth factor-β1, connective tissue growth factor et fibrose pulmonaire". Dijon, 2005. http://www.theses.fr/2005DIJOMU01.
Pełny tekst źródłaNorozian, Farnaz. "Transforming Growth Factor-β1 (TGF-β1) Induces Mast Cell Apoptosis". VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/1544.
Pełny tekst źródłaZuniga, Jorge E. "Binding properties and solution structure of the TGF-[beta] type I receptor extracellular domain : a dissertation /". San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1354133851&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Pełny tekst źródłaPan, Dejing. "Transforming growth factor-ß (TGF-ß) signaling in hematopoiesis and tumorigenesis /". Basel : [s.n.], 2008. http://edoc.unibas.ch/diss/DissB_8513.
Pełny tekst źródłaRose, Aidan Michael. "Transforming growth factor-beta signalling in human cutaneous squamous cell carcinoma". Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/51b1a1c1-ac43-4f60-aa77-9002af3f2186.
Pełny tekst źródłaGonçalves, Josiane de Oliveira. "Comparação entre os resultados da expressão gênica da desmina, alfa-actina e TGF-beta1 obtidos a partir dos métodos da reação em cadeia de polimerase via transcriptase reversa (RT-PCR) semiquantitativa e em tempo real (qRT-PCR) no modelo". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-15082014-163708/.
Pełny tekst źródłaThe mechanisms responsible for liver fibrosis in childhood are poorly understood. Children suffering from biliary atresia, when submitted to the successful Kasai portoentostomy, become anicteric, but nonetheless develop cirrhosis in the long term. Similarly, the occurrence of intrahepatic biliary stenosis in the postoperative period of liver transplantation may lead to cirrhosis of the whole organ. Such facts suggest that endocrine or paracrine mechanisms are involved in hepatic fibrogenesis. To elucidate this process, the selective bile duct ligation model in young rats was developed in our laboratory. Using this model, we identified changes in the expression of smooth muscle alpha-actin both in the obstructed parenchyma and the hepatic parenchyma adjacent to the obstruction. However, the expression profiles of desmin, a protein present at high levels during activation of hepatic stellate cells and TGF-beta1, the main pro-fibrogenic cytokine, were unchanged when analyzed with semiquantitative RT-PCR. Thus, the molecular mechanisms involved in the modulation of hepatic fibrogenesis in this experimental model are not fully understood. The methodology of qRT-PCR (real time PCR) has previously been described as a more precise and sensitive method, allowing the detection of increased copy number of the gene while amplification occurs, whereas by semiquantitative RT-PCR analysis transcripts is only perfomed after the amplification step. This study aimed to evaluate the molecular changes in experimental model of selective bile duct ligation and compare the results between semiquantitative RT-PCR and real-time qRT-PCR methods. Selective biliary duct ligation was performed on Wistar rats with 21 days of life, the groups were separated according to the moment of death: 7 or 60 days after surgery. The expression of desmin, alpha-actin smooth muscle and TGF-beta1 was examined in tissue from hepatic parenchyma with biliary obstruction (duct ligation - DL) and in the adjacent hepatic parenchyma (duct non-ligated - DNL) using semiquantitative RT-PCR and real-time qRT-PCR. The methodology of the real-time qRT-PCR allowed to identify changes in gene expression profile that were not shown by semiquantitative method. The DL parenchyma showed a more severe fibrogenic reaction, with increased alpha-actin smooth muscle and TGF-beta1 expression after 7 days. The DNL parenchyma presented a later fibrotic response, with increased desmin expression 7 and 60 days after surgery, besides of increased alpha-actin smooth muscle 60 days after surgery. Real-time qRT-PCR was more sensitive to identify changes in gene expression profile comparated to the semiquantitative method. Our results help to clarify the dynamic of molecular changes involved in the modulation of hepatic fibrogenesis in an experimental model of selective bile duct ligation and can be directly applied to the study of intrahepatic biliary stenosis and biliary atresia
Chen, Feng. "Phosphorylation and activation of transforming growth factor beta (TGF-[beta]) receptor kinases". Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/41406.
Pełny tekst źródłaOn t.p., "[beta]" appears as the lower case Greek letter. Vita.
Includes bibliographical references (leaves 166-207).
by Feng Chen.
Ph.D.
DUVERNELLE, CATHERINE. "Regulation de l'expression du tgf-1 (transforming growth factor-beta1) dans l'asthme". Université Louis Pasteur (Strasbourg) (1971-2008), 2000. http://www.theses.fr/2000STR13139.
Pełny tekst źródłaBailie, Janice Roberta. "The synthesis and biological activity of EFG/TGF-#alpha# fragments". Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335455.
Pełny tekst źródłaMaurice, Diane Barthelemie Emile. "The role of transforming growth factor-β in thymocyte development and T cell function". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271324.
Pełny tekst źródłaRodgers, Stephen D. "Characterizing the motogenic response of human keratinocytes to epidermal growth factor and transforming growth factor-alpha". Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/40610.
Pełny tekst źródłaKöhler, 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.
Pełny tekst źródłaVo, BaoHan Thi. "Nodal and transforming growth factor-β (TGF-β) signalings in prostate cancer cells". DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2013. http://digitalcommons.auctr.edu/dissertations/500.
Pełny tekst źródłaCzubala, Magdalena Anna. "Transforming growth factor-beta (TGF-β) induces HIV-1 restriction in Langerhans cells". Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/77792/.
Pełny tekst źródłaMoore, Lakisha Dionne. "Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/ldmoore.pdf.
Pełny tekst źródłaCheung, Ronald Se-Yuen. "Contrasting tumorigenic growth interactions of apoptosis-deficient MYC alleles with Transforming Growth Factor-alpha /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5000.
Pełny tekst źródłaSerwe, 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.
Pełny tekst źródłaKariyawasam, Harsha Hemantha. "Airway remodelling and transforming growth factor (TGF)-β superfamily signalling in allergen-induced asthma". Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/8641.
Pełny tekst źródłaKaruyawasan, Harsha Hemantha. "Airway remodelling and transforming growth factor (TGF)-B superfamily signalling in allergen-induced asthma". Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497534.
Pełny tekst źródłaFrankel, Sara. "The role of transforming growth factor-alpha in the human corpus luteum". Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295876.
Pełny tekst źródłaWhite, Robin Elaine. "Manipulation of Astrocytes After Spinal Cord Injury Using Transforming Growth Factor Alpha". The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259160724.
Pełny tekst źródłaZhang, Xuemei. "Src Kinase Signaling Regulates Connective Tissue Growth Factor (CTGF/CCN2) Induction by Transforming Growth Factor-Beta 1 (TGF-b1) in Osteoblasts". Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/63095.
Pełny tekst źródłaPh.D.
Connective tissue growth factor (CTGF/CCN2) is a cysteine rich, extracellular matrix protein that acts as an anabolic growth factor to regulate osteoblast differentiation and function. In osteoblasts, CTGF is induced by transforming growth factor beta 1 (TGF-β1) where it acts as a downstream mediator of TGF-β1 induced extracellular matrix production. The molecular mechanisms that control CTGF induction by TGF-β1 in osteoblasts are not understood. We have previously demonstrated the requirement of Src, Erk and Smad signaling for TGF-β1 induced CTGF promoter activity in primary osteoblasts, however the potential interaction among these signaling pathways in osteoblasts remains unknown. In this study, we demonstrate that CTGF is induced by TGF-β1 in rat osteosarcoma osteoblast like cells (ROS17/2.8). TGF-β1 activates Src and blocking of Src family kinases by PP2 abrogates TGF-β1 induced CTGF up-regulation. Western blot analysis revealed that primary osteoblasts and ROS 17/2.8 cells express not only Src, but also other Src family members, such as Fyn, Yes and Hck. In order to determine whether CTGF up-regulation is controlled by Src or other members, we used either kinase-dead dominant negative Src constructs in primary osteoblasts or Src siRNA in ROS17/2.8 cells to block Src function. Inactivation of Src by both kinase-dead and siRNA prevented TGF-β1 induced CTGF induction, demonstrating that TGF-β1 induced CTGF up-regulation is mediated only by Src not by other members. In addition, we also demonstrated that Erk is activated by TGF-β1 and that blocking of Erk activation using pharmacological inhibitors, PD98059 and U0126, prevents TGF-β1 induced CTGF induction, demonstrating the requirement of Erk for CTGF induction. These results prompted us to further explore the cross-talk between Src, Erk and Smads in ROS17/2.8 cells. Inhibition of Src using PP2 prevented Erk activation, demonstrating that Src is upstream of Erk. To investigate how Src and Erk regulate the canonical TGF-β1 signaling pathway, including Smad2/3 phosphorylation and nuclear translocation of activated Smads, we treated cells with TGF-β1 in the presence or absence of the Src inhibitor, PP2, or the Erk inhibitors, PD98059 or U0126. PP2 pre-treatment prevented the phosphorylation of Smad2/3 at both the SSXS motif and the linker region and consequently blocked their nuclear translocation, demonstrating that Src can regulate Smad signaling. In contrast, the Erk inhibitors did not have any effects on Smad phosphorylation and/or nuclear translocation. To examine whether Erk can modulate Smad signaling indirectly through the activation/ inactivation of required nuclear coactivators/ co-repressors that mediate Smad DNA binding, we used electro-mobility shift assays. These experiments showed that inhibition of Erk activation impaired transcriptional complex formation on the Smad binding element (SBE) and TGF- β responsive element (TRE) of the CTGF promoter, demonstrating that Erk activation is required for SBE and TRE transactivation. Taking together, these data demonstrate that Src is an essential upstream signaling transducer for Erk and Smad signaling in osteoblasts, and that while the Smad and Erk signaling cascades appear to function independent of each other, they are both essential for the formation of a transcriptionally active complex on the CTGF promoter.
Temple University--Theses
Young, Vicky Jane. "The role of the peritoneum and transforming growth factor β in the aetiology of endometriosis". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21099.
Pełny tekst źródłaDecologne, Nathalie. "Fibrose pleurale expérimentale : rôle de transforming growth factor (TGF)-β1 et des agents anticancéreux (bléomycine)". Dijon, 2008. http://www.theses.fr/2008DIJOMU07.
Pełny tekst źródłaLinks between pleura and fibrosis are important. Apart from pleurodesis, visceral pleura can be the site of severe fibrosis leading to fibrothorax associated with a high morbidity. Subpleural parenchyma is also the anatomical region of idiopathic pulmonary fibrosis (IPF) initiation although no link has been established between both. We developed a model of severe and progressive pleural fibrosis, induced by adenovirus-mediated gene transfer of Transforming Growth Factor (TGF)-β1 to mesothelial cells. In this model, collagen accumulation within the pleura but also within the subpleural parenchyma is the result of the transformation of mesothelial cells into myofibroblasts (mesothelio-fibroblastoid transformation -MFT-). This suggests the involvement of pleural mesothelium not only in pleural fibrosis but also possibly in IPF. We also studied the role of carbon nanoparticles (CN, carbon black), ultrafine particles found in ambient pollution or cigarette smoke, on fibrosis induced by bleomycin (BL), a cytotoxic agent known for its fibrotic side effects on human lungs. We showed that CN do not worsen BL-induced pulmonary fibrosis whereas BL+CN co-administration is needed to induce pleural fibrosis. This fibrosis is, as in the first model, progressive and characterized by collagen deposition within the pleura and the subpleural parenchyma. Our in vitro work on primary mesothelial cells confirms the key role of these cells in fibrogenesis. This innovative work on pleural fibrogenesis could lead to therapeutic applications for pleural fibrosis and even maybe IPF by using mesothelial cells as target
Ruf, Doris Anne. "Die Entwicklung der Pankreasfibrose im TGF-beta-1-transgenen Tiermodell". [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-57128.
Pełny tekst źródłaRichter, Audrey. "Studies on the interaction of the epidermal growth factor receptor with epidermal growth factor and transforming growth factor alpha to aid development of a growth factor antagonist". Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387049.
Pełny tekst źródłaWong, Soo Hang 1971. "Characterization of transforming growth factor-beta (TGF-_) receptor profiles on human dermal microvascular endothelial cells". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33041.
Pełny tekst źródłaMead, Anna Louise. "Modulation of transforming growth factor beta (TGF beta) and conjunctival scarring after glaucoma filtration surgery". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444824/.
Pełny tekst źródłaBall, Corbie. "The Role of Transforming Growth Factor Beta Signaling in Inflammation-Dependent Colon Cancer". Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/593463.
Pełny tekst źródłaHerckelrath, Tanja. "Genexpressionsmuster nach Behandlung von Hepatomzellen mit dem Cytokin TGF-beta bzw. mit Tumorpromotoren". [S.l. : s.n.], 2004. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11482176.
Pełny tekst źródłaNguyen-tat, Marc-Daniel. "Analyse der Auswirkungen von TGF-beta auf den Cadherin-Catenin-Adhäsionskomplex in den epithelialen Karzinomzelllinien SW-480 und MCF-7". [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-56542.
Pełny tekst źródłaHenning, Kirsten. "TGF-beta induzierte Expression extrazellulärer Matrixproteine durch Herzmuskelzellen der adulten Ratte". Giessen VVB Laufersweiler, 2009. http://geb.uni-giessen.de/geb/volltexte/2009/7319/index.html.
Pełny tekst źródłaLieber, Matthew Joshua. "Immunological Crosstalk between Human Transforming Growth Factor-β1 and the Malaria Vector Anopheles stephensi". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/42816.
Pełny tekst źródłaMaster of Science
Cheung, Ho-ki, i 張可琪. "Detection and characterization of transforming growth factor beta (TGF-?) and betaglycan in porcine and human milk". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29275805.
Pełny tekst źródłaYi, Sheng. "Transforming growth factor beta 1 modulates electrophysiological parameters of vas deferens epithelial cells". Diss., Kansas State University, 2013. http://hdl.handle.net/2097/16898.
Pełny tekst źródłaDepartment of Anatomy and Physiology
Bruce Schultz
Transforming growth factor β1 (TGF-β1) is a cytokine that reportedly affects the severity of cystic fibrosis lung disease. The goal of this project was to define the effect of TGF-β1 on vas deferens, an organ that is universally affected in male cystic fibrosis patients. In the first study, experiments were conducted using freshly isolated porcine vas deferens epithelial cells. Primary porcine vas deferens epithelial cells exposed to TGF-β1 exhibited a significantly reduced basal transepithelial electrical resistance (Rte). TGF-β1-induced reduction in Rte was prevented by SB431542, a TGF-β receptor I inhibitor, indicating that the effect of TGF-β1 requires the activation of TGF-β receptor I. Western blot and immunohistochemistry results showed the expression of TGF-β receptor I in native vas deferens epithelia, indicating that the impaired barrier function and anion secretion that were observed in cultured vas deferens cells can likely be observed in the native context. Immunohistochemical outcomes showed that TGF-β1 exposure led to loss of organization of tight junction proteins occludin and claudin-7. These outcomes suggest that TGF-β1 impairs the barrier integrity of epithelial cells lining the vas deferens. In a parallel study that employed PVD9902 cells that are derived from porcine vas deferens, TGF-β1 exposure significantly reduced anion secretion stimulated by forskolin, forskolin/IBMX, and 8-pCPT-cAMP, suggesting that TGF-β1 affects downstream targets of the cAMP signaling pathway. Real-time RT-PCR and western blot analysis showed that TGF-β1 exposure reduced both the mRNA and the protein abundance of cystic fibrosis transmembrane conductance regulator (CFTR). Pharmacological studies showed that the inhibitory effect of TGF-β1 on forskolin-stimulated anion secretion was abrogated by SB431542 and attenuated by SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor. These outcomes suggest that TGF-β1, via the activation of TGF-β receptor I and p38 MAPK signaling, reduces CFTR expression, and thus impairs CFTR-mediated anion secretion. Outcomes from these studies suggest that, in epithelial cells lining the vas deferens, TGF-β1 exposure leads to an impaired physical barrier and/or reduced anion secretion, which is expected to modify the composition and the maintenance of the luminal environment and thus, is expected to reduce male fertility.