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Dissertations / Theses on the topic 'Transforming growth factors'

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Published: 4 June 2021

Last updated: 1 August 2024

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1

Chung, Seung-Wook. "Modeling and analysis of the transforming growth factor beta signaling pathway." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 115 p, 2008. http://proquest.umi.com/pqdweb?did=1597632591&sid=15&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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2

Porteous, C. "Epidermal growth factor, α-transforming growth factor and breast cancer". Thesis, University of Aberdeen, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383650.

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Evidence exists that epidermal growth factor (EGF) and alpha transforming growth factor (αTGF) are important in breast cancer. An inverse relationship between epidermal growth factor receptor (EGF-R) and oestrogen receptor (ER) has been reported by some, (1) but not all workers (2). The aim in this thesis was to develop assays to measure, levels of EGF, and determine EGF-R status in human breast tumours. These results were then correlated with each other, with ER and node status and histological grade (Bloom & Richardson). An additional aim in this thesis was to develop a source of αTGF in conditioned median (CM) from a transformed cell line. After extraction and purification, the αTGF was intended for use as an immunogen to produce a polyclonal antiserum which could be used in either an RIA or ELISA. EGF was measured by a radioimmunoassay (RIA) utilising a rabbit antimouse EGF antiserum. This assay (sensitivity 0.1ng/ml) was demonstrated to have no cross reactivity with αTGF. The EGF-R assay was similar to that described by Sainsbury. (1) In a series of 88 human breast tumours 47 (53.4%) were found to contain extractable EGF. Forty eight (54.5%) were EGF-R positive and 39 (44.3%) were ER positive. A direct relationship between EGF and ER+ ve status was found (p < 0.01). Significantly higher levels of EGF were extracted from ER+ ve tumours (p = 0.049) compared with that from ER-ve tumours. However no relationship between EGF-R and EGF or ER status was found, or between EGF levels and histological grade or node status. A suitable cell line which produced αTGF, was obtained and culture conditions optimised. Alpha-TGF was assayed by a radioreceptor assay which utilised a cell line rich in EGF-R (A431). Extraction of αTGF was based on the principles of molecular grading by gel filtration (Sephadex G50), and ion exchange (Sephadex CM C25). By this process the αTGF was purified and separated it from any EGF present. By this method 20μg of αTGF was produced from 61t of CM. 1) Sainsbury JRC, Farndon JR, Serbet GV, Harris AL. Epidermal-growth-factor-receptors and oestrogen receptors in human breast cancer. Lancet 1985; <i>1</i>: 364-368. 2) Fitzpatrick SL, Brightwell J, Wattliff JL, Barrows GH, Schultz GS. Epidermal growth factor binding by breast tumour biopsies and relationship to oestrogen receptor and progestin receptor levels. Cancer Res 1984; <i>44</i>: 3448-3453.

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3

Smith, Cheryl A. "Skeletal muscle injury, fibrosis and transforming growth factor-[beta]." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1744.

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Thesis (Ph. D.)--West Virginia University, 2000.<br>Title from document title page. Document formatted into pages; contains xii, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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4

Gu, Ye. "Homo & heterodimeric TGF-[beta] family growth factors." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610106.

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5

Lanxon-Cookson, Erinn Claire. "Lovastatin decreases TGF-ß1 concentration of glomerular endothelial cells cultured in high glucose." Online access for everyone, 2008. http://www.dissertations.wsu.edu/Thesis/Spring2008/e_lanxon_cookson_040308.pdf.

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6

Zhang, Min Fen. "The role of milk transforming growth factor-[beta](TGF-[beta]) in the development of the infant gut and gut mucosal immune system." Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phz51.pdf.

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In title, [beta] is represented by the Greek letter. Copies of author's previously published articles inserted. Errata pages pasted onto back end-paper. Bibliography: leaves 104-137. Studies milk TGF-[beta] and its receptors in the post-natal gut using a rat model to investigate a link between milk TGF-[beta] and the development of the infant gut and gut mucosal immune system. Finds maternal milk may be a major source of TGF-[beta] to the immature gut and may react with receptors on the cells of the mucosal immune system along the gastro-intestinal tract, modulating infant mucosal immune responses in the transition to the post-natal enteral feeding.

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7

Pascal, M. M. "The role of transforming growth factor beta and other growth factors in the development of diabetic retinopathy." Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.593270.

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The present study showed that TFG-β mRNA and protein expression is regulated by glucose concentration in HREC. Maximal secreted protein levels and mRNA were produced at a concentration of 15 mM and the majority of the TGF-β is found in an active form in these cells. These results were novel and specific as HREC have not been shown before to express TFG-β in response to glucose. TGF-β appears to be central to a wide range of pathological features involved in the disease and this first study highlights a possible important role for TGF-β in the mechanism of induction of microvascular abnormalities in the retina. It could also play a role as a key mediator of the high glucose induced effects in DR, as is the case in the kidney. Glucose dependent changes in TGF-β receptors expression and signalling intermediates were also examined in HREC. These studies indicate that glucose is able to regulate both TGF-β expression and the receptor numbers of affinity but it is apparent that there is no simple correlation between secreted TGF-β and receptor number or affinity or expression. Protein kinase C isoforms protein expression did not change relatively to glucose but various isoforms were expressed at different intensities in endothelial cells and TGF-β signalling cascade involves a MAPK independent pathway. TGF-β expression in the ganglion cell layer demonstrated a neurotrophic role for TGF-β, whereas VEGF expression did not seem to correlate spatially or temporally with angiogenesis. We suggest that both systemic cells (PBLs) and endothelial cells are able to secrete a wide range of growth factors when activated by glucose. These factors, along with other ones (platelet derived growth factor or insulin like growth factor type 1), may act in synergy to produce an imbalance in growth factor levels which could lead to angiogenesis and therefore contribute to the pathogenesis of PDR.

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8

Kam, Siu-kei Christy. "The role of TGF-[beta] signaling in the initiation of TNF-[beta] expression in human PBMC derived macrophages." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38746049.

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9

Kam, Siu-kei Christy, та 甘笑琪. "The role of TGF-{221} signaling in the initiation of TNF-α expression in human PBMC derived macrophages". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38746049.

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10

Ni, Xueying. "Activin and a putative novel activin receptor-like kinase in the human placenta." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ39215.pdf.

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11

Tajsić, Tamara. "Nuclear envelope proteins modulate Transforming growth factor β superfamily signalling". Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610759.

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12

Chaudhury, Arindam. "Transforming growth factor-beta (TGFß)-mediated post-transcriptional regulation of epithelial-mesenchymal transdifferentiation (EMT)." Cleveland, Ohio : Cleveland State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1268963035.

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Thesis (Ph.D.)--Cleveland State University, 2010.<br>Abstract. Title from PDF t.p. (viewed on April 15, 2010). Includes bibliographical references (p. 151-187). Available online via the OhioLINK ETD Center and also available in print.

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13

Liu, 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.

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14

Helterline, Deri Lila Icenoggle. "Embryonic and tissue-specific regulation of myostatin-1 and -2 gene expression in zebrafish." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Thesis/Spring2006/d%5Fhelterline%5F050106.pdf.

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15

Liu, Ye. "Generation and utilization of knockout mice to elucidate the functions of the TGF-[beta] pathway in mammalian endodermal specification and placental development." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1158673346.

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16

Festing, Maria Helen. "Generation of novel conditional and hypomorphic alleles of the Smad2 gene and the effects of Smad2 removal in environments with elevated retinoid signaling." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1180467148.

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17

Wu, Xuewei, and 吴雪伟. "Isthmin, a novel extracellular regulator in nodal signaling pathway." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://sunzi.lib.hku.hk/hkuto/record/B45586573.

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18

Mei, Jie, and 梅節. "The physiological role of transforming growth factor-beta in gastrointestinal development in the pig." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29960861.

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19

Glinsmann-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.

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The human pancreatic cancer cell line T3M4, is known to produce transforming growth factor-alpha (TGF-alpha); as well as overexpress the receptor for this ligand, epidermal growth factor (EGF) receptor. TGF-alpha messenger RNA (mRNA) levels were assayed using northern blot, after addition of epidermal growth factor or TGF-alpha. The level of TGF-alpha mRNA was found to increase 2-fold at 2 hours and then return to near basal levels at 10 hours, after treatment with either ligand. Both ligands were also equipotent in a 2 hour dose response assay, with half maximal stimulation seen at 1 nM and maximal stimulation reached at 4 nM. Furthermore, there appeared to be a 2-fold increase in TGF-alpha transcription as determined by nuclear runoff experiments. Induction of TGF-alpha mRNA coupled with the overexpression of the EGF receptor, may result in a potent autocrine cycle; which may be found in other cancers.

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20

Emmanuel, Catherine. "Apoptotic And Morphometric Synergies Between Tumour Necrosis Factor-A And Transforming Growth Factor-B1 For Human Endothelial Cells." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/4864.

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21

Boelaert, Kristien. "Pituitary tumor transforming gene (PTTG) and related growth factors in endocrine tissues." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424097.

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22

Lam, 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.

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23

Fong, Sitt Wai. "The effects of transforming growth factor-β2 on synaptic transmission at the mammalian neuromuscular junctions". Thesis, University of Aberdeen, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=133996.

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Transforming growth factor-βs (TGF-βs) are highly expressed in neural development but why the adult nervous system continues to express them is unclear. TGF-β2 is concentrated at mature neuromuscular junctions (NMJs) of mammalian skeletal muscle fibres, and the nerve terminal expresses TβR-II receptors. To test the role of TGF-β2 at mammalian NMJs, I performed four experiments. The first study tested whether TGF-β2 acutely modulates synaptic transmission at mature mammalian NMJs. Second, I asked if chronically reduced TGF-β2 expression disrupts synaptic transmission. Third, I asked if TGF-β2’s effects differ in terminals adapted to different activity patterns in vivo. Lastly, I asked whether TGF-β1, a related peptide to TGF-β2, is distinct in terms of its effects on transmitter release. Using single electrode potential recording, I found TGF-β2 significantly increased the amplitude of spontaneous released single neurotransmitter vesicles (miniature endplate potentials, MEPPs) and nerve stimulation evoked multi-vesicular release (endplate potentials, EPPs). These effects were blocked by L-vesamicol, a vesicular acetylcholine transporter inhibitor, and bafilomycin, a proton pump inhibitor, suggesting the increase in MEPP/EPP amplitude is due to increased vesicle filling presynaptically. These effects were also blocked by the MARK inhibitors, UO126 and PD98059, suggesting TGF-β2 acts via a MARK-dependent pathway. Postsynaptically, two electrode recording showed postsynaptic potential amplitude was enhanced by an increased fibre input resistance, suggesting TGF-β2 also acts postsynaptically. TGF-β2 reduced the number of vesicles released per stimulus (quanta content, QC) but this was blocked by atropine, showing this was indirect through autoreceptor negative feedback. Voltage clamp recording showed TGF-β2 significantly increased the miniature end plate currents (MEPCs), but not the end-plate currents (EPCs), supporting my initial hypothesis that TGF-β2 acts mainly presynaptically to increase vesicle filling. In TGF-β2+/- mice, I found greater MEPP amplitude variability. This supports my previous findings that TGF-β2 modulates vesicle filling. Unexpectedly, there was an excess in larger MEPP sizes (>0.88 mV), perhaps reflecting upregulation of either presynaptic signalling or another synaptic mediator. Two MEPP amplitude populations were induced in TGF-β2-treated TGF-β2+/- mouse NMJs, similar to the bimodal vesicle population in electroplaques. The extensor digitorum longus (EDL, ~95% fast fibres) and soleus (SOL, ~95% slow fibres) were used to investigate whether the TGF-β2-mediated effect differed between fibre types. Overall, TGF-β2 increased the quantal size (MEPP amplitude) in NMJs of both muscles, suggesting this effect is not fibre-type specific and, together with results in mice, that the TGF-β2-mediated increase in vesicle filling is common to all mammalian neuromuscular terminals. With respect to EPP amplitude and QC, the results differed between muscles. In EDL, the EPP amplitude was not significantly changed, whereas it increased in SOL. In EDL, QC was reduced but not in SOL. These difference compared to diaphragm perhaps do reflect muscle fibre-type dependent differences. TGF-β1, at 0.1 ng/ml, significantly reduced quantal size – the opposite of TGF-β2 at any concentration. One explanation would be that a receptor inhibition by TGF-β1 at low concentration interferes with endogenous TGF-β2 binding/receptor activation at the NMJ. However, when the TGF-β1 concentration was raised to 1 ng/ml, like TGF-β2, it significantly increased MEPP amplitude. This suggests that perhaps sufficient binding of TGF-β1 results in the receptor activation of TGF-β2 like signalling. Overall, I conclude that TGF-β2 enhances the size of spontaneous synaptic potentials in all types of muscle fibres, and this is much more rapid (1 hr vs 1 day) than at central neurone synapses in culture. Detailed study in the rat diaphragm shows it increased the evoked EPP amplitude, reduced QC and increased postsynaptic input resistance. Together, TGF-β2 would therefore enhance the postsynaptic depolarisation increasing synaptic strength, and by reducing QC, increase the efficiency of neurotransmission at mammalian NMJs. While unimportant for single stimuli in healthy terminals, by conserving vesicle use, it may help maintain release during stimulus trains, especially during neuromuscular disease.

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24

O'Keeffe, Fiona. "The effects of Pitx3 and GDF-5 on the generation and survival of midbrain dopaminergic neurons." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610732.

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25

Cheung, Ho-ki, and 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.

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26

Lee, B. C. Bob. "Probing the molecular mechanisms of how polymorphisms in Cerberus-like result in low bone mineral density." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39711481.

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27

Sheils, Emma. "The TGF-β signalling pathway in Trichinella spiralis : phylogenetic and functional analysis of TGF-β ligands". Thesis, University of Aberdeen, 2011. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=184012.

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The release of genome sequence information is revolutionising the study of helminth parasites by providing important datasets for comparative genomics, allowing the comprehensive analysis of signalling pathways that regulate nematode development. Much of the current knowledge of nematode signalling pathways is based on studies of the free-living model Caenorhabditis elegans. The recent availability of the Trichinella spiralis genome sequence presented an opportunity to study signalling pathways of this, and other, parasitic nematodes, providing a phylum-wide overview of a given signalling pathway. The transforming growth factor-β (TGF-β) ligands are a superfamily of structurally related polypeptides that regulate a wide range of cellular processes in animal tissues. Since the discovery that the TGF-β daf-7 regulates the developmentally-arrested dauer stage in C. elegans, there is the potential for TGF-β signalling to regulate developmental arrest, parasite development and even host-parasite communication in T. spiralis and other nematodes. In the present study, thirteen genes encoding putative TGF-β signalling components, from T. spiralis, have been identified and characterised. Phylogenetic analysis suggests that daf-7 is not conserved beyond C. elegans and that functional extrapolation from C. elegans biology to distantly-related nematodes is difficult. Furthermore, the analysis herein shows a high level of divergence among parasitic nematode TGF-βs. Since the last common ancestor of T. spiralis and C. elegans was the ancestor of the entire nematode phylum, these comparisons allow speculation on the TGF-β signalling networks of the ancestral nematode and provide information on the emergence of TGF-β signalling in animals. ES products from T. spiralis are shown to be capable of interacting directly with mammalian cell receptors and utilise their receptors to control gene expression in vitro. This presents the possibility that these TGF-β ligands may play a part in the formation and maintenance of the host-parasite complex.

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28

Wang, Feng. "The role of TGFBI in development and cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610043.

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29

Odhiambo, John F. "Evaluation of weaning regimen and seminal plasma biology on reproductive management in cattle." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=6057.

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Thesis (Ph. D.)--West Virginia University, 2008.<br>Title from document title page. Document formatted into pages; contains ix, 122 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 99-122).

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30

Wang, Qian. "Role of growth factors in regulating of lens fibre differentiation." Thesis, The University of Sydney, 2008. https://hdl.handle.net/2123/28141.

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The lens is a good developmental biology model owing to its simplicity and distinct polarity. The anterior lens compartment constitutes a monolayer of cuboidal-shaped epithelial cells, which overly a mass of precisely aligned elongated fibre cells. Lens growth throughout life is mediated by proliferation of epithelial cells and their subsequent differentiation into fibres, to form a transparent and tightly-packed lens. During lens growth and development, cell proliferation is mainly restricted to a specialised region at the periphery of the lens epithelium known as the gerrninative zone. The progeny of these cell divisions migrate posteriorly into the transitional zone, where they initiate their differentiation into the lens fibre cells. Based on this, the lens epithelial cells can therefore be regarded as the progenitors of the lens fibre cells. The fate of lens cells is regulated by growth factors found in the ocular environment, the aqueous and vitreous humour, which bathes the lens anteriorly and posteriorly, respectively. Growth factors in vitreous regulate lens differentiation by activating intracellular signalling pathways, which lead to the expression of fibre-specific proteins. However, the mechanism by which growth factors regulate lens fibre differentiation has yet to be elucidated. In order to investigate the mechanisms involved in promoting cell differentiation, the present study characterised the downstream signalling pathways induced by a range of growth factors and compared these to those induced by the vitreous humour, the source of these endogenous growth factors. Using this approach, we showed that two major signalling pathways, the ERKl/2 and Pl3—K/Akt signalling, are required for lens fibre differentiation, with the duration of ERKl/Z phosphorylation determining lens cell fate: transient ERKl/2 phosphorylation being associated with lens cell proliferation and sustained ERKl/2 phosphorylation being required for lens fibre differentiation. In addition, a combination of growth factors in Vitreous are thought to contribute to the distinct ERKl/2 and PI3-K/Akt signalling required for lens fibre differentiation. Furthermore, in lens cells, we identified a negative regulator of the ERK1/2 signalling pathway, Spry2, which may be important for defining the cell fate. Overexpression of Spry2 in vitro and in vivo can block cell elongation during lens fibre differentiation. Taken together, the findings presented in this thesis illustrate that the lens fibre differentiation process is complex and is regulated by multiple signalling pathways activated by various growth factors and is effectively monitored by intracellular signalling regulators.

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31

Woodward, Terry L. "Inhibition of cellular proliferation by retinoids and transforming growth factor-betas in bovine mammary cells correlates with increased connexin43 expression." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40283.

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Bovine fibroblasts and epithelial cells were isolated from surgically biopsied mammary tissue. Characterization of population doubling time, cytoskeletal intermediate filaments, cryopreservation survival, and viability were performed on all fibroblast and epithelial cells. Several clonal fibroblast cell lines were cotransfected with a plasmid bearing the SV-40 Large-T-antigen, and the pSV-2 neo plasmid. Transfected cells were subsequently selected with G418 sulfate and cloned.<br>MAC-T cells and non-clonal primary bovine mammary epithelial cells proliferated in response to IGF-I, insulin, serum and serum albumin. MAC-T cells did not proliferate when cultured in EGF, estrogen, progesterone, estrogen+progesterone, growth hormone, prolactin, and only modest proliferation was obtained after TGF-$ alpha$ treatment. Subsequent experiments used serum, insulin or IGF-I (and its analogues) to stimulate cellular proliferation. Serum albumin was not added to serum-free media preparations since it stimulated cellular proliferation.<br>TGF-$ beta$ receptors were characterized in MAC-T cells and normal fibroblasts. Affinity labelling studies revealed that MAC-T and MF-2 cells contained type I, II, and III autoregulatable receptors. Fibroblast proliferation, was inhibited 50% by TGF-$ beta$. TGF-$ beta$ inhibited MAC-T cellular proliferation at concentrations among the lowest ever reported, ED$ sb{ rm 50}$ = 4 pm. TGF-$ beta$ was not cytotoxic at concentrations 1000-fold higher.<br>Retinoic acid (RA) also inhibited proliferation of MAC-T cells. Inhibition of proliferation did not occur when cells were growth stimulated by IGF-I analogues that do not bind IGFBPs. Unlike TGF-$ beta$, RA treatment increased IGFBP-2 and decreased IGFBP-3 protein expression by cells into media and on the cell's membrane. RA was cytotoxic at concentrations 10-fold higher than ED$ sb{100}$.<br>Fibroblasts and epithelial cells expressed the gap junction (GJ) protein, connexin43, with transformed fibroblasts expressing significantly less connexin43. Perinuclear and cell surface connexin43 was immunodetected in epithelial and fibroblasts cells. TGF-$ beta$, RA or cAMP, increased connexin43 protein expression, especially phosphorylated species. Only cAMP noticeably altered immunolocalization patterns of connexin43, causing a shift from perinuclear pools to the cell surface. None of the growth inhibitors affected GJ communication as measured by dye transfer. Therefore, mammary epithelial cells are growth inhibited by TGF-$ beta$ and RA by distinct mechanisms and both growth inhibitors significantly enhance the gap junction protein, connexin43, without increasing GJ communication.

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To, Man-yan. "Potential oncogenic role of FOXGI in ovarian cancer." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557856.

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Yan, Qi. "Regulation of retinal endothelial cells and pericytes by VEGF, TGF-beta1, and SPARC /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/5686.

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Kong, Pui-ching Christie. "Nucleocytoplasmic shuttling of Smad7 that plays paradoxical roles in hepatocellular carcinoma." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B44226883.

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35

林詩敏 and 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.

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36

Liu, Chi 1963. "Transforming growth factors produced by normal and neoplastically transformed rat liver epithelial cells in culture." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63768.

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37

Wang, Qian-Shu. "Alterations in Transforming Growth Factors and G1 Cyclins in N- Nitrosomethylbenzylamine-Induced Rat Esophageal Tumorigenesis /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487935125881887.

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38

Ekrikpo, Udeme Ekpenyong. "Chronic kidney disease in HIV populations: prevalence, risk factors and role of transforming growth factor beta (TGF-߀1) polymorphisms." Doctoral thesis, Faculty of Health Sciences, 2019. https://hdl.handle.net/11427/31740.

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Background and purpose: With the advent of antiretroviral therapy, HIV-infected individuals now live longer and are at increased risk of chronic kidney disease (CKD). Also, recent studies indicate a genetic predisposition to CKD in the African HIV population. This work investigated the prevalence of CKD (and its correlates) in the global and local HIV population and proceeded to investigate the diagnostic utility of urinary transforming growth factor-beta-1 (TGF-β1) for CKD in the HIV population and determine the association between polymorphisms of TGF-β1 gene and prevalent CKD. Methods: A meta-analysis was performed to document the prevalence of CKD in the global HIV population. From the local HIV population in Nigeria, the prevalence of CKD and traditional risk factors for cardiovascular disease was determined. Using ELISA, TGF-β1 levels was assayed in the urine samples of HIV patients with or without CKD to investigate the ability of urinary TGF-β1 to diagnose early CKD. SNP genotyping of rs1800469, rs1800470, rs1800471, rs121918282 in TGF-β1, rs60910145 (APOL1), rs73885319 (APOL1), rs71785313 (APOL1) and rs743811 (HMOX1) was performed using predesigned TaqMan genotyping assays. Results: Using meta-analytic methods, the global pooled CKD prevalence was 6.4% (95%CI 5.2–7.7%) with MDRD, and 4.8% (2.9–7.1%) with CKD-EPI. Among the WHO regions, Africa had the highest MDRD-based prevalence, 7.9% (5.2-11.1%) with the West African subregion carrying the heaviest burden, 14.6% (9.9- 20.0%). Among the local HIV population, using the CKD-EPI equation, the prevalence of CKD was 13.4% (11.6- 15.4%). Hypertension prevalence was 26.7% (25.5-28.0%); diabetes 5.6% (4.5-6.7%); obesity 8.3% (7.6-9.1%) and dyslipidaemia 29.1% (26.1-32.1%). HIV-infected individuals with CKD had significantly higher levels of urinary TGF-β1-creatinine ratio (uTGFβ1Cr) after controlling for potential confounding factors in regression models. However, within the CKD-HIV group, uTGFβ1Cr reduced as CKD stage worsened. The presence of APOL1 genetic risk independently increased the risk of CKD (OR 2.54, 95% CI 1.44-4.51) in the HIV population while the TGF-β1 SNP, rs1800470, appeared to have a protective effect (OR 0.44 (95% CI 0.20-0.97). There was no significant association between HMOX1 SNPs and CKD occurrence. Conclusion: There is a high prevalence of CKD (and other cardiovascular risk factors) in the adult HIVpopulation. Urinary TGF-β1 may be useful in the non-invasive detection of early CKD in the HIV population. Genetic testing may be used to predict the risk of CKD in the HIV population.

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Lee, Yin-yin Candice. "The role of thrombospondin-1 in the synthesis and activation of TGF-[beta]1 in human proximal tubular epithelial cells under elevated glucose concentrations /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31596010.

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Rohe, Benjamin G. "Regulation of 1,25D(3)-MARRS expression by TGFB1 in a rat intestinal epithelial cell line." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 4.38 Mb., 108 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:1435850.

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Mace, Peter, and n/a. "Biochemistry of ovine bone and morphogenetic proteins and receptors." University of Otago. Department of Biochemistry, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.133410.

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The transforming growth factor (TGF)-β superfamily mediates a wide range of differentiation and developmental processes across many genera. GDF9 and BMP15 are expressed exclusively in the mammalian ovary and are the only TGF-β ligands that lack the conserved cysteine residue used for dimerisation. As a platform for studying the interactions between GDF9 and BMP15 and their receptors, BMPRII and BMPRIb, a variety of strategies were attempted to produce soluble and active proteins from recombinant systems. Both ligands and receptors showed a tendency to form insoluble aggregates when expressed in prokaryotic systems; however after extensive screening, quantities of biologically active GDF9 were produced using in vitro refolding. When expressed alone, either containing a histidine tag or as an untagged protein, the BMPRII ectodomain was deposited as insoluble inclusion bodies. This protein, subjected to in vitro refolding procedures, exhibited multiple species following anion exchange chromatography and size exclusion chromatography, as visualised on native PAGE. Separation of these species could be achieved using a MonoP matrix. One of these separated fractions, representing about 5% of the starting material, was amenable to crystallisation, and furthermore exhibited activity in a rat granulosa cell thymidine incorporation assay. Two different crystals forms of the extracellular domain of BMPRII were grown from the same protein batch under similar crystallisation conditions. Notably, the tetragonal form that grew more slowly possessed several disordered finger regions, while electron density for the entire molecule was clear in the orthorhombic form. The hydrophobic core of the ligand binding surface of BMPRII , as seen in both structures, resembles that of ActRII bound to BMP2. The A-loop of BMPRII, which is involved in ligand binding, lies in two different conformations in the two structures of BMPRII, mediated by a rearrangement in disulfide Cys94-Cys117. It is proposed here that the tetragonal form represents the ligand-bound receptor structure. Although the majority of the hydrophobic binding surface is shared with ActRII(b), it is likely that His87 and Tyr40 are unique residues that confer specificity in BMPRII ligand binding.

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Guo, Hong. "Molecular therapy for peritoneal fibrosis targeting the TGF-b/Smad signaling pathway /." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557509.

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Guo, Hong, and 郭紅. "Molecular therapy for peritoneal fibrosis: targeting the TGF-{221}/Smad signaling pathway." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557509.

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Lee, B. C. Bob, and 李卜駿. "Probing the molecular mechanisms of how polymorphisms in Cerberus-likeresult in low bone mineral density." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793771.

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Herbert, 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.

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Allende, Marie Alexandra. "Blood vessel growth in primate retinal development relationship of retinal maturation with choriocapillaris growth and a role for TGF-ß in the retina /." Connect to full text, 2008. http://hdl.handle.net/2123/4145.

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Thesis (Ph. D.)--University of Sydney, 2008.<br>Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Department of Clinical Ophthalmology and Eye Health, Faculty of Medicine. Title from title screen (viewed Apr. 8, 2009) Includes bibliography. Also available in print form.

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Laurens, Ilze. "Development of a new extraction method for platelet-rich plasma and partial purification of platelet-derived growth factor and transforming growth factor beta." Diss., University of Pretoria, 2013. http://hdl.handle.net/2263/40717.

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Platelet-rich plasma (PRP) is the cell free plasma, which has an enriched concentration of platelets and clotting factors with the ability to enhance the natural healing process. PRP is often used by physicians in an office setting to accelerate the healing of a variety of sports related injuries, chronic wounds and enhance skin rejuvenation. PRP mimics the wound healing cascade by enhancing the recruitment, proliferation and differentiation of cells involved in tissue regeneration. Although PRP is used to enhance healing, the efficacy thereof is debated as no clear-cut set of parameters is available that device manufacturers and protocols should follow. The lack of uniformity in the PRP preparation methods results in differing PRP volume, platelet contents and unavoidably platelet-derived growth factors. Therefore, the aim of this study was to develop a simple and rapid method for preparing autologous PRP in an office setting using a tabletop centrifuge for point-of-care use. The simplified preparation procedure involved a single centrifugation step of 18 ml of whole blood, which sufficiently enriched the platelet content in the PRP fraction. As activated platelets express and release growth factors and cytokines that mediate the different phases of the wound healing cascade, the extracted PRP fraction was activated with an ethanol, calcium chloride (CaCl2) and platelet poor plasma (PPP) preparation in glass containers, without the collection of additional blood as required in some protocols. The activated PRP formed a fibrin clot, trapping the degranulating platelets and its released growth factors. The concentration of TGF- 1 obtained from the fibrin clot was 45.49 ± 3.80 ng/ml, in range with the available literature. During the in vitro studies, the extracted PRP by the developed method was able to significantly induce cell proliferation in a dose dependent manner. Cells enumerated with the crystal violet assay indicated that the cells treaded with 5% or 10% PRP significantly increased the percentage of viable cells to 165-176% and 156-158%, when compared to the positive controls. Cells enumerated with the MTT-assay indicated that the cells treaded with 5% or 10% PRP increased the percentage of viable cells to 79-91% and 87-105% which is comparable to that of the positive control. Data from the cellular proliferation assays indicate that sufficient plateletderived growth factors had been obtained with the preparation procedure. Furthermore, data from the in vivo studies indicated that the extracted PRP was able to augment soft tissue regeneration and bone formation. Treatment with the activated PRP resulted in symptom reduction and accelerated healing of various injuries. The simplified preparation and the use of the provided study product packaged in a kit developed during this study will enable physicians to easily obtain autologous PRP, in an office setting for point-of-care use, with the ability to induce tissue regeneration.<br>Dissertation (MSc)--University of Pretoria, 2013<br>gm2014<br>Pharmacology<br>unrestricted

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陳嘉威 and Ka-wai Patrick Chan. "Transforming growth factor-{221}1 induces cell invasiveness via the downregulation of junctional adhesion molecule-A." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47151602.

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Hester, Mark Edward. "Utilization of gene knockout approaches in the mouse to elucidate additional functions of smad proteins during mammalian development." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1118656704.

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Thesis (Ph. D.)--Ohio State University, 2005.<br>Title from first page of PDF file. Document formatted into pages; contains xv, 137 p.; also includes graphics. Includes bibliographical references (p. 122-137). Available online via OhioLINK's ETD Center

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Popescu, Olivia. "Characterization of Dante, a novel member of the DANCerberus family TGF-[beta] inhibitors." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80856.

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TGFbeta signaling peptides have been shown to play increasingly diverse roles in metazoan development and tissue homeostasis. Negative regulation of TGFbeta ligands such as Nodal can be achieved by physical interactions with inhibitory molecules. Dante is a recently identified putative member of DAN/Cerberus family of TGFbeta inhibitors. Previously shown to be unilaterally expressed on the right side of the mouse node, Dante has been suggested to play a role in Left-Right axis formation possibly by inhibition of Nodal molecules. The aim of this study was to further characterize Dante and to determine whether it can physically interact with Nodal. First, a longer Dante cDNA was isolated in an attempt to clone the full-length transcript. Furthermore, Dante expression pattern was analyzed during murine development and adult tissues. Lastly, co-immunoprecipitation experiments demonstrated that Dante is able to physically interact with Nodal, providing further support for its potential role as a Nodal inhibitor.

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