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Teses / dissertações sobre o tema "Insulin-like growth factor-binding proteins"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 26 de julho de 2024

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1

Robertson, James Gray. "Insulin-like growth factors and insulin-like growth factor binding proteins in wounds /". Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phr6509.pdf.

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2

Hopkins, Nicholas John. "Insulin-like growth factor-I and its binding proteins". Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240702.

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3

Clark, Sarah Jane. "The growth hormone, insulin-like growth factor, insulin-like growth factor binding proteins and insulin axis in acute liver failure". Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397943.

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4

Jones, Tiffany Celeste. "Syndecan-4 binds insulin-like growth factor binding protein-4". Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/jones.pdf.

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5

Mireuta, Matei. "Aspects of insulin-like growth factor binding proteins in cancer". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114128.

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The insulin-like growth factor (IGF) system is composed of two ligands (IGF-1 and IGF-2), two receptors (IGF-1R and IGF-2R) and six binding proteins (IGFBP-1 to -6). IGFs act as endocrine, paracrine and autocrine growth factors and stimulate cell growth, proliferation and metabolism. There is extensive evidence, both from in vitro and in vivo models as well as population studies, that IGF physiology is relevant to neoplasia. IGF-1R is the physiologic receptor for both ligands and its activation elicits a plethora of changes at the cellular level, such as activation of PI3K/AKT/mTOR and Ras/Raf/MAP kinase pathways. Given its role in the maintenance and promotion of neoplasia, the IGF system represents a potential target in the context of cancer therapy.Classically, IGFBPs have been described as carrier proteins for IGFs in the blood and other fluids. They can regulate IGF bioavailability both positively through increases in ligand half-life as well as negatively through competition with the IGF-1R for ligand binding. In addition to their classical roles, there is evidence suggesting that IGFBPs can act independently of IGFs by poorly characterized mechanisms. Additionally, epidemiologic studies have correlated overexpression of certain IGFBPs, in particular IGFBP-2, with poor prognosis in various cancers.Although the role of IGFBPs has been extensively studied in the context of both normal and malignant growth, this thesis describes several new aspects of IGFBPs in neoplasia. In the second chapter, we study the effect of the PI3K/AKT/mTOR cascade on IGFBP-2 gene expression in a breast cancer cell line in vitro. We demonstrate that activation of this pathway essentially leads to an Sp1-dependent increase in IGFBP-2 gene transcription. We further show that Sp-1 is phosphorylated upon PI3K/AKT/mTOR pathway activation and accumulates in the nucleus. In the third chapter, we study the effects of 2-deoxyglucose (2-DG) on IGF-1:IGFBP-3 complex formation. A recent publication suggested that 2-DG unexpectedly disrupted IGF-1:IGFBP-3 binding leading to increases in IGF-1R and AKT signaling in various cell lines. We show by three different techniques that neither 2-DG nor glucose affect IGF-1:IGFBP-3 complex formation. We additionally show that the 2-DG effects observed are not consistent between cell lines and likely the result of changes in intracellular signaling. In the fourth chapter, we study the effects of a novel therapeutic antibody (BI836845) with high affinity for both IGF-1 and IGF-2. In mouse serum samples ex vivo, we show that the addition of BI836845 leads to a shift of IGF-1 from the IGFBPs to the antibody. In vivo, we demonstrate that BI836845 binds the vast majority of IGF-1. Finally, we demonstrate that BI836845 induces a decrease in IGFBP-3 and an increase in growth hormone levels in C57 BL/6 mice.
L'ensemble du système de facteurs de croissance insulinomimétique (IGF) est composé de deux ligands (IGF-1 et IGF-2), de deux récepteurs (IGF- 1R et IGF-2R) et de six protéines de liaison (IGFBP-1 à 6). Les IGFs sont des hormones endocrines, paracrines et autocrines qui stimulent la croissance cellulaire, la prolifération et le métabolisme. Il existe un grand nombre d'études utilisant des approches épidémiologiques ou des modèles in vivo et in vitro qui démontrent l'importance des IGFs dans le contexte du cancer. Le IGF-1R est le récepteur physiologique des deux ligands et son activation mène à d'importants changements cellulaires tels que l'activation des voies de signalisation PI3K/AKT/mTOR et Ras/Raf/MAPK. Étant donné son rôle dans la promotion et dans la progression du cancer, le système des IGFs représente une cible potentielle pour le traitement du cancer. De façon classique, les protéines de liaison IGFBP ont été décrites comme de simples porteurs d'IGFs dans le sang et autres fluides. Les IGFBPs peuvent modifier la biodisponibilité des IGFs de façon positive en augmentant leur demi-vie ou de façon négative due à leur compétition avec le IGF-1R pour la liaison. En plus de leur rôle classique, il est de plus en plus évident que ces protéines peuvent agir de manière indépendante, mais les mécanismes impliqués restent flous. Également, il existe des études épidémiologiques qui ont corrélé la surexpression de IGFBPs, en particulier IGFBP-2, avec un pronostic défavorable dans plusieurs formes de cancer. Bien que le rôle des IGFBPs ait été largement étudié dans le contexte de la croissance normale et en néoplasie, la présente thèse révèle quelques nouveaux aspects de la physiologie des IGFBPs dans le contexte du cancer. En première partie, nous étudions l'effet de la voie de signalisation PI3K/AKT/mTOR sur l'expression du gène IGFBP-2 dans une lignée cellulaire de cancer du sein. Nous démontrons que l'activation de cette voie mène essentiellement à une augmentation de la transcription de ce gène de manière dépendante au facteur de transcription Sp-1. De plus, nous établissons que Sp-1 est phosphorylé par l'activation de la voie PI3K/AKT/mTOR et s'accumule dans le noyau. En deuxième partie, nous étudions les effets de la molécule 2-deoxyglucose (2-DG) sur la liaison entre IGF-1 et IGFBP-3. Un récent article avait suggéré un effet inhibitoire de cette molécule sur la formation de complexes IGF -1 :IGFBP-3. Nous démontrons par trois méthodes différentes que 2-DG ou la molécule apparentée glucose n'ont aucun effet sur la liaison entre IGF-1 et IGFBP-3. De plus, nous démontrons que les effets cellulaires de 2-DG sur l'activation de la voie PI3K/AKT/mTOR observées par les auteurs de l'article en question ne sont pas universels et sont probablement le résultat de signaux intracellulaires. Finalement, en dernière partie, nous étudions les effets d'un nouvel anticorps thérapeutique nommé BI836845 qui possède une grande affinité pour IGF-1 et IGF-2. Dans des échantillons de sérum de souris ex vivo, nous démontrons que l'ajout de BI836845 déplace IGF-1 des complexes naturels contenant les IGFBPs vers des complexes contenant l'anticorps. In vivo, nous démontrons que BI836845 lie la grande majorité d'IGF-1. Nous démontrons aussi que l'anticorps mène à une baisse de la concentration de IGFBP-3 et à une hausse de la concentration de l'hormone de croissance chez des souris C57 BL/6.

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6

Twigg, Stephen Morris. "Insulin-like growth factor binding protein-5 and its complexes". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27686.

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The insulin-like growth factors, IGF-I and IGF-H, are multifunctional proteins. They are anabolic and they regulate glycaemia, and at tissue and cellular level, IGFs are mitogenic and anti—apoptotic and they may modify differentiated cell function. In serum and tissues IGF bioactivity is modified by six well characterised insulin-like growth factor binding proteins (IGFBPs), that have high affinity for IGF-I and IGF-II.

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7

Milner, Steven John. "The oxidative folding of insulin-like growth factor-I analogues /". Title page, table of contents and summary only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phm65945.pdf.

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8

Nickerson, Tara. "A role for insulin-like growth factor binding proteins in apoptosis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ50229.pdf.

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9

Lucic, Melinda Robin. "Characterisation of the molecular interactions between insulin-like growth factors and their binding proteins". Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phl9375.pdf.

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Addenda inserted in back. Includes bibliographical references (leaves 139-160) Assesses the importance of amino acids 221 to 236 of bIGFBP-2 for IGF binding activity, by creating amino acid substitutions.

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10

de, los Rios Patricia. "Insulin-like growth factor binding proteins (IGFBPs) in ovine fetal growth plate chondrocytes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0011/MQ28557.pdf.

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11

Weber, Miriam S. "The Role of Insulin-like Growth Factor-I and IGF-binding Proteins in Mammary Gland Development". Diss., Virginia Tech, 1998. http://hdl.handle.net/10919/29457.

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Development of the mammary gland is likely mediated by locally produced growth factors acting in concert with circulating mitogens. To investigate the importance of mammary synthesis of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBP), the initial objective was to evaluate the physiological effects of recombinant IGF-I synthesis in the mouse mammary gland. Expression of recombinant IGF-I was targeted by the mouse mammary tumor virus - long terminal repeat (MMTV-LTR) to the mammary glands of two lines (15 and 29) of transgenic mice. Mammary synthesis of recombinant IGF-I increased the frequency of appearance of mammary alveolar buds (71% vs. 21%) in transgenic compared with non-transgenic CD-1 mice. During lactation, mammary synthesis of recombinant IGF-I reduced the amount of endogenous native IGF-I secreted into milk of transgenic mice. Regardless of transgenesis, a shift in the milk IGFBP profile from predominantly IGFBP-3 to a lower molecular weight IGFBP occurred between d 8 and d 12 of lactation. The altered composition of milk from transgenic line 29 dams reduced by 27% the average daily gain of suckling litters, compared with CD-1 dams. Moreover, mammary glands of transgenic mice were less regressed after weaning than controls and were characterized by the presence of more organized secretory lobules. The second overall objective was to evaluate the regulation and physiological effects of mammary IGF-I and IGFBP synthesis in prepubertal heifers. Serum and extracts of mammary tissue at 5% concentration in media stimulated DNA synthesis 545% and 28%, respectively, in primary mammary epithelial organoids in collagen gel culture. Addition of IGFBP-3 strongly inhibited this growth response. High feeding level tended to increase IGFBP-3 levels in mammary tissue and reduced by 30% the growth response to mammary tissue extracts. Somatotropin increased the mitogenic response to mammary extracts at high feeding level and increased the tissue content of IGF-I by 46%. In summary, local synthesis of IGF-I and IGFBP is influenced by feeding level and exogenous somatotropin and contributes substantially to effects on mammary cell proliferation. Interactions of locally produced IGFBP-3 with IGF-I and other growth factors appear to be especially important when mammary growth is modulated by feeding level.
Ph. D.

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12

Burk, John Robert. "Insulin-like Growth Factor Binding Proteins in the Plasma of Growing Horses". Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31712.

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Insulin-like growth factor binding proteins (IGFBP) are modulators of insulin-like growth factor I (IGF-I), which functions as a regulator of cartilage and bone development. Rapid growth and high starch diets have been associated with increased circulating concentrations of IGF-I, which lead to developmental orthopedic disorders in foals. The objective of this study was to assess the effects of age, diet, growth and season on plasma IGFBP and IGF-I concentrations from birth to 16 mo of age in Thoroughbred foals. Twenty-two mares maintained on mixed grass/legume pasture were randomly divided into two dietary groups and fed either a high starch and sugar supplement (SS) or a starch-restricted fiber and fat supplement (FF) for 3 mo prior to and after foaling. Monthly blood samples were obtained from SS and FF foals up to 16 mo of age and analyzed for IGF-I using an RIA and IGFBP using western ligand blot analysis. Auxilogical measurements of foals were also obtained each month. The effect of diet, month, and diet*month interactions upon the subject horse (diet) were analyzed using a mixed model with repeated measures, and correlations of normally distributed data were calculated using Pearsonâ s correlation. Six IGFBP bands of molecular weights 109, 39, 36, 35, 34, and 33 kDa were identified in foal plasma. Doublet bands were recognized at 109, 39, and 35 kDa, however they were not all believed to be singular pure IGFBP. A band with a molecular weight of 213 kDa was observed and presumed to be a ternary complex of IGFBP-3, IGF-I, and an acid labile subunit. The IGFBP 109 kDa has been previously recognized as a band unique to the equine, it was not a singular pure IGFBP because of its high molecular weight. No effect of diet on plasma IGFBP was found in individual sampling of yearlings, but an effect of month was noted when testing May - August 2001 against May - August 2002 in pooled plasma samples with concentrations of the IGFBP 39 kDa increasing (P < 0.0003). In contrast, concentrations of the IGFBPâ s 33, 34 and 36 kDa decreased (P < 0.003, P < 0.0002, and P < 0.0003 respectively). Environmental effects were noted upon IGFBPâ s 33, 36, 39, and 109 kDa (P < 0.003, P < 0.001, P < 0.04, and P < 0.01) with a temperature*daylength interaction. Correlations existed between ADG and IGFBP 33 (r = 0.64; P < 0.0001), 34 (r = 0.40; P < 0.0001), 35 (r = 0.33; P < 0.0006), 36 (r = 0.47; P < 0.0001), and 39 kDa (r = - 0.18, P < 0.02). A correlation was also found between IGF-I and ADG (r = 0.11; P < 0.04), confirming the previously reported relationship of IGF-I in growth rate of foals. These results underline the importance of characterizing the activity of IGFBPâ s in relation to growth, age and season when interpreting changes of the somatotropic axis. Further, the increase in certain IGFBPâ s and simultaneous decrease in others stress the need for further research on the tissue specific modulating effects that IGFBPâ s have on IGF-I.
Master of Science

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13

Carrick, Francine Ellen. "Characterization of bovine insulin like growth factor binding protein-2 : structure and function". Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phc3158.pdf.

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14

Wang, Jing. "Novel insulin-like growth factor-binding protein proteases: detection and characterization /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-942-4/.

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15

Chan, Yue-sin. "Insulin-like growth factor I and linear growth at birth to five days in rats". Thesis, Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B24873354.

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16

Hobba, Graham D. "Studies to identify and characterise IGF-binding determinants of IGFBP-2 /". Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phh6814.pdf.

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17

Watanabe, Shin. "Insulin-like growth factor axis (insulin-like growth factor-I/insulin-like growth factor-binding protein-3) as a prognostic predictor of heart failure: association with adiponectin". Kyoto University, 2011. http://hdl.handle.net/2433/142074.

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18

Nanayakkara, Sachith N. "The role of IGF-1 and hormone binding proteins in understanding insulin-associated equine laminitis". Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/118300/1/Sachith_Nanayakkara_Thesis.pdf.

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Laminitis is a common and extremely painful hoof disease in horses. We know that it is caused by abnormally high levels of insulin, but the mechanism of insulin action is not known. One theory is that insulin over-stimulates the receptors for a related hormone, insulin-like growth factor-1, and that this leads to uncontrolled cell proliferation in the hoof, which ultimately causes the disease. The first part of the thesis examines this theory, by determining if insulin can activate IGF-1 receptors directly, or displace IGF-1 from its binding proteins in blood, thereby increasing the activity of IGF-1. Because some horses appear to be naturally resistant to developing insulin-induced laminitis, the second part of the thesis examines if these horses carry proteins in their blood that can bind to insulin and reduce its activity.

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19

Kallincos, Nicholas Campbell. "Growth hormone (GH) and insulin-like growth factor-I (IGF-I) in vivo: investigation via transgenesis in rats /". Adelaide : Thesis (Ph.D.) -- University of Adelaide, Department of Biochemistry, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phk143.pdf.

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20

Miyamoto, Shinichi. "Matrix Metalloproteinase-7 Facilitates Insulin-like Growth Factor Bioavailability through its Proteinase Activity on Insulin-like Growth Factor Binding Protein-3". Kyoto University, 2004. http://hdl.handle.net/2433/147465.

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21

Alsabban, Abdulrahman Essam. "Establishing methods to screen novel small molecules targeting insulin-like growth factor/insulin-like growth factor binding protein interaction". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45046.

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Insulin-like growth factors (IGFs) are important systemic mediators of growth and survival that suppress apoptosis and promote cell cycle progression, angiogenesis and metastatic activities in various cancers by activating IGF-IR tyrosine kinase-mediated signaling. These effects depend on the bioavailability of IGFs, which is regulated by IGF binding proteins (IGFBPs). Increased IGFBP-2 and IGFBP-5 expression observed in castration-resistant prostate cancer is thought to promote tumor progression by enhancing IGF-mediated signaling. IGFBPs have cooperative carboxy-terminal and amino-terminal low and a high affinity IGF binding sites. I hypothesize that blocking the high affinity IGF binding site can affect the bioavailability of IGFs to target tissues and thus be used for treatment of various IGF-responsive diseases including prostate cancer. I initially characterized immunologic reagents capable of being used in sandwich ELISA formats to detect IGF-I and IGFBP-5 and attempted several configurations to establish an IGF-I/IGFBP-5 “bridged” sandwich ELISA platform to measure association and dissociation of IGF-I/IGFBP-5 complex formation. The inability of all bridged ELISA formats tested to measure IGF-I/IGFBP-5 binding, lead me to developed a Bio-Layer Interferometry-based assay that measures IGF-I/ IGFBP-5 binding kinetics that will allow for screening of factors that can affect this intermolecular interaction. I demonstrated that biotinylated IGF-I bound to streptavidin-coated biosensors can be used to measure binding of recombinant IGFBP-5 [2.24 nm shift in optical density (Response)]. I also demonstrated that IGF-I could efficiently disrupt this interaction (0.21 nm shift), while the amino-terminal IGF-I mutant, E3R, exhibits an intermediate competitive activity (1.47 nm shift) and insulin exhibits a low competitive activity (1.83 nm shift). In addition, I demonstrated that IGF-I can competitively disrupted this interaction, resulting in a dissociation rate constant (Kdis 1.5-³ 1/s), In contrast, the amino terminal IGF-I mutant, E3R binds with an intermediate affinity (Kdis 5.6-⁴ 1/s), and buffer free sample results in a (Kdis) of 1.5-⁴ (1/s). These results demonstrate the capacity of this BLI-based assay to differentiate relative competitive activity of compounds that target the high affinity IGF-I binding site of IGFBPs and establish a platform to screen for factors that might be developed as rationale therapeutics to disrupt sequestration of IGF-I by IGFBPs.

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22

Lord, Andrew P. D. "IGF transfer from blood to tissue: comparison of IGF-I with analogs that bind poorly to binding proteins, using a vascular perfusion model : a thesis submitted to the University of Adelaide, South Australia, for the degree of Doctor of Philosophy /". Title page, abstract and table of contents, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl866.pdf.

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23

Martin, Katrin. "Untersuchungen der Insulinähnlichen Wachstumsfaktoren IGF-I und IGF-II, deren Bindeproteine IGFBP-2 und IGFBP-3 und der Säurelabilen Untereinheit ALS bei Kindern mit soliden Tumoren". [S.l. : s.n.], 2007.

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24

Balderson, Stephanie D. "Investigations of Insulin-Like Growth Factor I Cell Surface Binding: Regulation by Insulin-Like Growth Factor Binding Protein-3 and Heparan Sulfate Proteoglycan". Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/30494.

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The primary aim of this text is to gain insight on how cellular activation by a insulin-like growth factor (IGF-I), in the presence of insulin-like growth factor binding protein-3 (IGFBP-3), is influenced by heparan sulfate proteoglycans (HSPG). Initial research will be presented, assumptions and hypotheses that were included in the development of mathematical models will be discussed, and the future enhancements of the models will be explored. There are many potential scenarios for how each component might influence the others. Mathematical modeling techniques will highlight the contributions made by numerous extracellular parameters on IGF-I cell surface binding. Tentative assumptions can be applied to modeling techniques and predictions may aid in the direction of future experiments. Experimentally, it was found that IGFBP-3 inhibited IGF-I Bovine Aortic Endothelial (BAE) cell surface binding while p9 HS slightly increased IGF-I BAE cell surface binding. IGFBP-3 has a higher binding affinity for IGF-I (3 x 10-9 M) than p9 HS has for IGF-I (1.5 x 10-8 M) as determined with cell-free binding assays. The presence of p9 HS countered the inhibiting effect of IGFBP-3 on IGF-I BAE cell surface binding. Although preliminary experiments with labeled p9 HS and IGFBP-3 indicated little to no cell surface binding, later experiments indicated that both IGFBP-3 and p9 HS do bind to the BAE cell surface. Pre-incubation of BAE cells with either IGFBP-3 or p9 HS resulted in an increase of IGF-I BAE cell surface binding . There was a more substantial increase of IGF-I surface binding when cells were pre-incubated with IGFBP- 3 than p9 HS. There was a larger increase of IGF-I BAE cell surface binding when cells were pre-incubated with p9 HS than when p9 HS and IGF-I were added simultaneously. This suggests that IGFBP-3 and p9 HS surface binding plays key role in IGF-I surface binding, however, p9 HS surface binding does not alter IGF-I surface binding as much as IGFBP-3 surface binding seems to. Experimental work helps further the understanding of IGF-I cellular activation as regulated by IGFBP-3 and p9 HS. Developing mathematical models allows the researcher to focus on individual elements in a complex systems and gain insight on how the real system will respond to individual changes. Discrepancies between the model results and the experimental data presented indicate that soluble receptor inhibition is not sufficient to account for experimental results. The alliance of engineering analysis and molecular biology helps to clarify significant principles relevant to the conveyance of growth factors into tissue. Awareness of the effects of individual parameters in the delivery system, made possible with mathematical models, will provide guidance and save time in the design of future therapeutics involving growth factors.
Master of Science

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25

Ahlsén, Maria. "Insulin-like growth factor binding protein-3 : structure and function /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-350-4/.

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26

Ye, Siying. "Molecular characterization of insulin-regulated aminopeptidase (IRAP) /". Connect to thesis, 2006. http://eprints.unimelb.edu.au/archive/00001651.

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27

Whellams, Emma Jane. "The role and regulation of insulin like growth factor binding proteins in arthritis". Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324333.

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28

Forbes, Briony Evelyn. "Characterization and purification of insulin-like growth factor-binding proteins of human fibroblasts /". Title page, contents and summary only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phf692.pdf.

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29

Schaffer, Andrea. "Insulin-like growth factor-I, insulin-like growth factor binding protein-3 and the risk of cervical squamous intraepithelial lesions". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81435.

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Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) have been associated with an increased risk of several cancers. This case-control study investigated the relationship between IGF-I and IGFBP-3 plasma levels and the risk of squamous intraepithelial lesions (SILs) of the cervix, as well as the risk of HPV infection in women. 366 cases and 366 controls were recruited from five Montreal area hospitals. There was a significantly decreased risk of LSIL for the highest quartile of IGFBP-3 relative to the lowest quartile (Odds Ratio (OR)=0.25, 95% confidence interval (CI) 0.08-0.77), adjusted for age, HPV status and IGF-I. Also, there was a significantly increased risk of being positive for HPV, specifically high-risk types, for the highest quartiles of IGFBP-3 relative to the lowest quartile in controls (OR=4.53, 95% CI 1.33-15.40), adjusted for age and IGF-I. IGF-I was not significantly associated with SILs or HPV infection.

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30

Gargosky, Sharron Erna. "Insulin-like growth factor (IGF) and IGF binding proteins during pregnancy in the rat and human /". Title page, table of contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phg2315.pdf.

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31

Carr, Jillian M. "Insulin-like growth factor binding proteins (IGFBPs) in growth and development of the ovine fetus". Adelaide Thesis (Ph.D.) -- University of Adelaide, Department of Biochemistry, 1994. http://hdl.handle.net/2440/21607.

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32

Gajanandana, Oraprapai. "Studies of complexes formed in blood in vivo between an insulin-like growth factor analog and binding proteins". Title page, contents and abstract only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phg145.pdf.

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Includes bibliographical references (43 leaves) This study shows that when LR3IGF-I is administered to animals in pharmacologically active doses, it may be present in either the free form or bound to IGF-binding protein(s) in the circulation. Age and nutrition which are factors that regulate synthesis of endogenous IGF-I and IGF-binding proteins, affect the in vivo formation of complexes between the analog and IGFBP(s). This study also suggests that IGFBP-1 inhibits the pharmacological activity of circulating LR3IGF-I on thymus whereas it appears to stimulate the pharmacological activity of LR3IGF-I in kidneys.

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33

Degger, Brian. "Fish insulin-like growth factors : their role in growth from a functional perspective". Thesis, Queensland University of Technology, 2001.

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34

Hassard, Jennifer. "Mitochondrial membrane binding and protein complexing of the anti-apoptotic adaptor protein Grb10". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33772.

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Grb10 is a member of the Grb7 family of adaptor proteins that also includes Grb7 and Grb14. These three members contain multiple protein binding domains and lack enzymatic activity. Extensive two-hybrid studies have demonstrated binding of Grb10 to numerous activated tyrosine kinase receptors including the insulin receptor (IR) and insulin-like growth factor-I receptor (IGF-IR), as well as many non-receptor molecules such as MEK1, Raf-1, and Nedd4. Grb10 has been implicated in IGF-I anti-apoptotic signaling regulation through interactions with Raf-1 and the mitochondrial membrane.
In this report the pattern of transient Grb10 translocation following IGF-I cellular stimulation was studied. This report also demonstrates the implication of a short variable amino-terminal region of Grb10 in mitochondrial membrane association. Finally, assays were developed with the goal of identifying new Grb10 binding partners.

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35

Lynch, Jill Ellen. "Functional studies of SCN2B over-expression in LNCaP human prostate cancer cells". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 103 p, 2008. http://proquest.umi.com/pqdweb?did=1481658511&sid=16&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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36

Le, Hang Thi Thu. "Functional characterization of IGF2BP2, a diabetes-susceptibility gene". Thesis, University of Cambridge, 2011. https://www.repository.cam.ac.uk/handle/1810/283871.

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37

Wright, Rebecca Jane. "Insulin-like growth factor binding proteins as co-ordinators of human ovarian follicular function". Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404588.

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38

Launchbury, R. "Insulin-like growth factor binding protein-3 and the hyperplastic prostate". Thesis, University of Edinburgh, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.653702.

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The role of insulin-like growth binding-protein-3 (IGFBP-3) was investigated in primary cultures of hyperplastic prostate cells in the hope of identifying novel drug targets. Benign prostatic hyperplasia (BPH) is a disease of the ageing male, the aetiology of which is unknown. Growth factors, such as insulin-like growth factor (IGF) are implicated in stimulating the prostate growth which causes hyperplasia. IGFBP-3 is an inhibitory binding protein, which functions to sequester IGF away from its receptor, but also has an IGF-independent action once fragmented. Cellular proteases, including prostate specific antigen (PSA), fragment IGFBP-3, and the resulting fragments have actions independent of the intact protein. The inhibitory action of fragmented IGFBP-3 has been documented in prostate epithelial cell lines, but there are no reports of its action in stromal cells, which is investigated here. Initially, the endogenous production of IGFBP-3 by primary cultures of stroma and epithelium was investigated. RT-PCR showed expression of IGFBP-3 mRNA in both stroma and epithelium, and immunocytochemistry, and Western blotting on cell lysates, indicated IGFBP-3 protein production in both cell types. The localisation of IGFBP-3 in primary cultures was the same as that observed in sections of hyperplastic and malignant prostate tissue. Western blotting on stromal and epithelial conditioned medium showed fragmentation of endogenous IGFBP-3 by cellular proteases. Proteolysis of IGFBP-3 by PSA produced fragments of 22-25kDa and 15kDa. ELISAs showed a large differential in concentration of IGFBP-3 produced by primary stomal and epithelial cells which affected subsequent growth experiments using exogenous protein. Proliferation experiments showed a non-dose dependent inhibitory response to IGFBP-3 by epithelial cells, probably due to sequestration of IGF. No response was observed in stomal cells to intact or fragmented protein, however, due to the high concentration of endogenous IGFBP-3 produced.

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39

Fowler, Clare Amanda. "Insulin-like growth factor binding protein modulation of breast cancer treatment". Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392972.

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40

Kallincos, Nicholas Campbell. "Growth hormone (GH) and insulin-like growth factor-I (IGF-I) in vivo: investigation via transgenesis in rats". Thesis, Adelaide, 1993. http://hdl.handle.net/2440/21602.

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41

Mukherjee, Sudipto. "Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/mukherjee.pdf.

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42

Bode-Rhoads, Michelle Lynn. "Regulation of the growth hormone receptor, insulin-like growth factor (IGF) I and IGF binding protein 2 in reproductive tissues of dairy cattle during lactation and associated effects on fertility". free to MU campus, to others for purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3164490.

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43

Hamilton, Fairley. "Regulation of sex hormone binding globulin and insulin-like growth factor binding protein-1". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243549.

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44

Gao, Shan. "Screen for proteins that regulate sensitivity to inhibition of the insulin-like growth factor 1 receptor". Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565965.

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The type 1 insulin-like growth factor receptor (lGF-1 R) plays a significant role in tumor growth and spread, and IGF-1 R inhibitors and antibodies are now undergoing clinical testing. However, factors that regulate sensitivity to IGF-1 R inhibition remain unclear. The aim of this project is to identify proteins whose depletion regulates sensitivity to IGF-1 R inhibition, in order to design effective combination treatments to benefit patients. An IGF-1 R kinase inhibitor, AZ12253801 (provided by AstraZeneca) was able to block IGF-induced phosphorylation of IGF-1 R in DU145 prostate cancer and MCF-7 breast cancer cells, inhibited downstream signalling in DU145 cells, and also inhibited proliferation and cell survival of both cell lines. AZ12253801 was used in an unbiased siRNA screen in both cell lines, using two s'iRNA libraries (779 kinase-related Kinome and 230 DNA repair-associated siRNAs). Eight Kinome and five DNA repair-associated hits have been identified after primary and second round screens, and further validated. The strongest hit was dishevelled homolog 3 (DVL3), a member of the WNT signalling pathway, which is highly expressed in both cell lines. DVL3 silencing caused reduction in active l3-catenin and inactivated the mTOR pathway, consistent with previous studies, and did not affect IGF-1 Rand AKT activity. However, DVL3 silencing led to activation of MEK1/2-ERK1/2 in serum-starved cells and sensitized this pathway to IGF-1 stimulation, with translocation of ERK1/2 into the nucleus and increased expression of ERK1/2 target genes. A DVL PDZ domain inhibitor (DVLi) showed similar effects on active l3-catenin, mTOR signalling and ERK1/2 signalling activity. The administration of DVLi increased sensitivity to AZ12253801 in cell lines with detectable ERK1/2 activation, but not prostate cancer cells in which ERK signalling was suppressed and AKT was activated in the context of loss of functional PTEN. Furthermore, DVL3 regulated activation of ERKs by influencing signaling downstream of the IGF-1 R and upstream of RAS, and DVL3 was found in a complex with the adaptor proteins GRB2 and DAB2. GRB2 knockdown was capable of abolishing ERK1/2 activation induced by DVLi, further implicating involvement of GRB2, and DAB2 silencing sensitized to IGF-1 R inhibition, mimicking effects of DVL3 depletion. Taken together, DVL3 silencing or inhibition enhances sensitivity to IGF-1 R inhibition by negatively regulating the ERK1/2 signaling pathway. These investigations shed new light on the factors that regulate IGF signaling, and provide a rational basis for design of clinical trials of IGF-1 R inhibitors.

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45

Niemann, Inga [Verfasser]. "Die Assoziation zwischen Insulin-like Growth Factor I sowie Insulin-like Growth Factor Binding Protein 3 und Knochenumbaumarkern in der Allgemeinbevölkerung / Inga Niemann". Greifswald : Universitätsbibliothek Greifswald, 2016. http://d-nb.info/1115357387/34.

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46

Eiberger, Edgar Ludwig Eugen. "Insulin-like Growth Factor I (IGF-I), IGF Binding Protein-3 (IGFBP-3) und Alkalische Phosphatase (AP) bei organischem Wachstumshormonmangel (GHD), intrauteriner Wachstumsretardierung und idiopathischem Kleinwuchs (ISS)". [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10732978.

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47

Gill, Zahidah Perveen. "Modulation of cellular survival by insulin-like growth factor binding protein-3". Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297809.

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48

Shah, Pooja Trusha Mehool. "Insulin-like growth factor binding protein-2 and its role in angiogenesis". Thesis, University of Leeds, 2018. http://etheses.whiterose.ac.uk/22866/.

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Therapeutic angiogenesis is currently under investigation to restore tissue perfusion in peripheral arterial disease (PAD). However, clinical trials have proved to be disappointing in stimulating the development of functional blood vessels and reducing adverse events. Insulin-like growth factor binding protein-2 (IGFBP-2) has demonstrated potential in proangiogenic activity but the molecular mechanisms remain unestablished. Structurally, IGFBP-2 possesses domains which can interact with insulin-like growth factor (IGF), receptor protein tyrosine phosphatase-β, glycosaminoglycans, integrins and can potentially translocate into the nucleus to activate cellular and pathological processes. In this project, we used two IGFBP-2 over-expressing mouse models, namely a global and an endothelial specific model, to determine whether increasing IGFBP-2 can increase perfusion in an experimental model of ischemia in vivo. The angiogenic potential of IGFBP-2 was investigated in an array of in vitro angiogenic signalling and functionality studies in vascular endothelial cells. Recombinant IGFBP-2 was generated, in which site-directed mutagenesis was employed to disrupt the integrin binding site (RGD), IGF binding site, or the heparin binding domain-1/nuclear localisation signal. These mutants were used to determine the primary mechanism IGFBP-2 may use to exert in vitro angiogenic effects. Upregulation of IGFBP-2 in ischemic muscles was confirmed in wild-type mice following hind limb ischemia surgery. IGFBP-2 over-expression significantly enhanced perfusion at early stages of recovery. In vitro angiogenic signalling and functional assays demonstrated IGFBP-2 increased phosphorylation of Akt and ERK/MAPK, as well as enhancing endothelial cell adhesion, wound closure and tube formation. Site-directed mutagenesis identified the RGD domain to be critical in IGFBP-2-stimulated in vitro angiogenic activity. In contrast to VEGF, exposure of IGFBP-2 to endothelial cells did not affect endothelial monolayer permeability. In conclusion, IGFBP-2, via its RGD domain displays promising potential as a new therapeutic angiogenic treatment.

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49

Berg, Ulrika. "The IGF-IGFBP system in aerobic exercise - with focus on skeletal muscle /". Stockholm : Institutionen för kvinnors och barns hälsa, Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-379-5/.

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50

Lin, Wan-Jung. "The nuclear actions of IGFBP-3". Online access for everyone, 2006. http://www.dissertations.wsu.edu/Thesis/Summer2006/w%5Flin%5F072606.pdf.

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