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Tesis sobre el tema "Utrophin"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 1 de febrero de 2022

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1

Broderick, Michael James Francis. "The utrophin-actin interface." Thesis, University of Glasgow, 2005. http://theses.gla.ac.uk/30889/.

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The spectrin superfamily is a diverse group of proteins variously involved in cross- linking, bundling and binding to the F-actin cytoskeleton. These proteins are modular in nature and interaction with actin occurs, at least in part, via CH domain containing ABDs. The actin binding domains of the spectrin superfamily proteins are all very similar in overall structure however the functions of the individual proteins differ greatly. Utrophin is a member of the spectrin superfamily and has been used extensively to investigate and model the association of actin-binding domains with F- actin; howev

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2

Dennis, Carina Louise. "Promoter studies of the utrophin gene." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320271.

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3

Pearce, Marcela. "Genomic structure of the human utrophin gene." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318897.

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4

Fisher, Rosie. "Utrophin in therapy of Duchenne muscular distrophy." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:192fbccd-d037-4ce8-b1cd-0315afe1860d.

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5

James, Marian. "Monoclonal antibody studies of dystrophin and utrophin." Thesis, University of Salford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360455.

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6

Moores, Carolyn Ann. "Structure-function analysis of the utrophin actin binding domain." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624459.

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7

Coriati, Adèle. "Skeletal Muscle Specific IRES Activity of Utrophin A Is Enhanced by Eef1a2." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19866.

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Understanding the regulatory mechanisms controlling utrophin A expression at the sarcolemma of dystrophic muscles will facilitate the development of therapeutic strategies to ameliorate the pathophysiological features of Duchenne Muscular Dystrophy (DMD). The main goal of this study was to characterize the regulation of utrophin A IRES activity using a transgenic mouse model expressing the utrophin A 5’UTR bicistronic reporter and to identify trans-acting factors that could mediate IRES activity and endogenous expression of utrophin A. We found that utrophin A IRES activity is specifically exp

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8

Péladeau, Christine. "Utrophin A Upregulation by FDA-Approved Drugs for the Treatment of Duchenne Muscular Dystrophy." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39298.

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Duchenne Muscular Dystrophy (DMD) is a disorder caused by mutations in the dystrophin gene, preventing the production of the functional dystrophin protein which assures maintenance of the myofiber integrity throughout muscle contraction. A lack of dystrophin results in severe muscle degeneration and regeneration accompanied by a loss of muscle function. Many pre-clinical and clinical studies are focused on developing strategies to counteract the detrimental effects of DMD; however, there is no cure. One such approach consists of upregulating the endogenous protein utrophin A in dystrophic musc

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9

Perkins, Kelly Joanne. "Molecular and functional analysis of the transcriptional regulation of utrophin." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270259.

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10

Wilson, James Baillie. "Transcription of the utrophin gene : identification and characterisation of novel transcripts." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392667.

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11

Bareja, Akshay. "Utrophin upregulation and microRNAs : two avenues of Duchenne muscular dystrophy therapy research." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:6a5145e9-7abf-4f86-bb8e-a3284125d99a.

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Characterized by the severe progressive wastage of skeletal muscle, Duchenne muscular dystrophy (DMD) is a crippling X-linked recessive disease that is caused by the absence of the protein dystrophin. This thesis aimed to critically evaluate the potential of different therapeutic options to combat this disease. Utrophin is a paralogue of dystrophin. The Fiona mouse is an mdx (dystrophin-deficient) transgenic mouse that overexpresses the full-length utrophin protein in skeletal muscle, and various studies have shown that it does not display a dystrophic phenotype. However, these studies have on

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12

Gramolini, Anthony Orlando. "Molecular mechanisms contributing to the expression of utrophin at the mammalian neuromuscular synapse." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/NQ57045.pdf.

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13

Gramolini, Anthony O. "Molecular mechanisms contributing to the expression of utrophin at the mammalian neuromuscular synapse." Thesis, University of Ottawa (Canada), 2000. http://hdl.handle.net/10393/9454.

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Duchenne muscular dystrophy (DMD) is the most severe and prevalent primary myopathy. This disease is characterized by repeated cycles of muscle fiber degeneration and regeneration with an eventual failure to regenerate leading to the progressive replacement of myofibers by adipose and connective tissues. The genetic defects responsible for DMD are mutations in the short arm of the X chromosome which prevent the production of normal size dystrophin, a large cytoskeletal protein of 427 kDa. In contrast to the homogeneous distribution of dystrophin along muscle fibers, utrophin preferentially acc

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14

Deconinck, Anne E. "Mouse models of neuromuscular disease." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320277.

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15

Wakefield, Philip M. "Gene therapy for duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365743.

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16

Economou, Androuila. "Generation of a mutation in the cysteine rich domain of the murine utrophin locus." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322572.

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17

Burton, Edward Alan. "Investigations of the transcriptional regulation of utrophin : potential therapeutic application in Duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312610.

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18

Ahmed, Aatika. "Combinatorial Utrophin A Activation in Muscle as a Therapeutic Strategy to Treat Duchenne Muscular Dystrophy." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/31911.

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Duchenne Muscular Dystrophy (DMD) is an X-linked recessive neuromuscular disorder caused by mutations or deletions in the dystrophin gene. Utrophin up-regulation therapy is among the various therapeutic strategies that are being investigated to treat DMD. In this strategy utrophin, a dystrophin homologue, is up-regulated along the entire length of the sarcolemma to replace the absent dystrophin protein. Previous studies have revealed that utrophin A expression can be controlled by various transcriptional, post-transcriptional and translational mechanisms and pharmacological modulation of these

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19

Al-Rewashdy, Hasanen. "Determining the Contribution of Utrophin A Versus Other Components of the Slow, Oxidative Phenotype in the Beneficial Adaptations of Dystrophic Muscle Fibers Following AMPK Activation." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31470.

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Duchenne Muscular Dystrophy (DMD) results from the absence of a functional dystrophin protein. Among its possible therapeutic options is the upregulation of dystrophin’s autosomal analogue, utrophin A. This can be achieved by a pharmacologically induced shift towards a slower, more oxidative skeletal muscle phenotype, which has been shown to confer morphological and functional improvements on models of DMD. Whether these improvements are a result of the utrophin A upregulation or other beneficial adaptations associated with the slow, oxidative phenotype, such as improved autophagy, has not bee

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20

Gainer, Thomas Gregory. "Immune Response Markers are Prevalent in the mRNA Expression Profile of Maturing Dystrophic Murine Skeletal Muscle." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/33263.

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Duchenne muscular dystrophy (DMD) is a severe and fatal muscle wasting disease characterized by a high mutation rate in the gene that encodes the membrane-associated protein dystrophin that results in absence of expressed protein. Although the primary genetic defect for DMD is known, the mechanisms that initiate the onset of DMD are not currently understood. This study tested the hypothesis that pathophysiological processes involved in DMD could be identified by the global expression of mRNA in maturing dystrophin- and utrophin-deficient mouse (mdx:utrn-/-) muscles. Two potential dystrophic o

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21

Vuorinen, Aini. "Towards the elucidation of the mechanism of action of small molecule upregulators of utrophin using chemical proteomics." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:8734b8c8-c48f-45bc-a5ee-0ecd6b27b978.

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22

Thompson, Jennifer Margaret. "The role of the 5'-untranslated region in regulating the expression of utrophin in skeletal muscle cells." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26541.

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Up-regulating utrophin expression at the sarcolemma is thought to be a key therapeutic approach in the fight against DMD. Utrophin was found to have two isoforms which differ mainly in their 5'-untranslated regions. Effects of the utrophin 5'UTRs on reportergene expression in cell culture and muscle injection experiments were assayed by measuring both reporter transcript and protein levels. Translation efficiencies were estimated by calculating transcript to protein ratios. Our results indicate that there is considerable translation inhibition in control muscle. In comparison, significantly di

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23

Schubert, Sandra. "The Role of [beta]2-Syntrophin Phosphorylation in Secretory Granule Exocytosis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1146851994562-42414.

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The trafficking of insulin secretory granules(SGs) of pancreatic b-cells is a tightly controlled complex network. Increasing evidence indicates that the cortical actin cytoskeleton modulates the mobility and exocytosis of SGs,yet the mechanisms anchoring SGs to the cytoskeleton is not completely understood.It has been shown by Ort et al.(2000,2001) that the cytoplasmic tail of an intrinsic membrane protein of the SGs named ICA512/IA-2 binds the PDZ domain of b2-syntrophin,which in turn binds to the F-actin-binding protein utrophin. These data also indicate that stimulation of SG exocytosis aff

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24

Chukwurah, George A. "Development of a stable expression vector system for gene transfer into sceletal muscle followinq detection of sequence instability in utrophin cDNA during cloning." Thesis, Royal Holloway, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521777.

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25

Schubert, Sandra. "The Role of [beta]2-Syntrophin Phosphorylation in Secretory Granule Exocytosis." Doctoral thesis, Technische Universität Dresden, 2005. https://tud.qucosa.de/id/qucosa%3A23710.

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The trafficking of insulin secretory granules(SGs) of pancreatic b-cells is a tightly controlled complex network. Increasing evidence indicates that the cortical actin cytoskeleton modulates the mobility and exocytosis of SGs,yet the mechanisms anchoring SGs to the cytoskeleton is not completely understood.It has been shown by Ort et al.(2000,2001) that the cytoplasmic tail of an intrinsic membrane protein of the SGs named ICA512/IA-2 binds the PDZ domain of b2-syntrophin,which in turn binds to the F-actin-binding protein utrophin. These data also indicate that stimulation of SG exocytosis aff

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26

Lessa, Thais Borges. "Estudo comparativo da contratilidade e das propriedades passivas do músculo diafragma do mdx, mdx/utrn+/- e C57Bl10 com diferentes idades." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-06062016-153503/.

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A Distrofia Muscular de Duchenne (DMD) é uma importante e severa doença músculo degenerativa causada pela mutação do gene da distrofina. Na ausência da distrofina, o sarcolema das células torna-se vulnerável devido a danos induzidos por ciclos contínuos de degeneração e regeneração. Consequentemente, a força muscular diminui e as miofibras são substituídas por tecido fibrótico. Dentre os músculos esqueléticos afetados, o diafragma, destaca-se por ser o principal músculo respiratório acometido na DMD. Similarmente a DMD humana, o modelo mdx, apesar de exibir um fenótipo suave, este apresenta um

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27

Woolf, Peter James. "Cardiac calcium handling in the mouse model of Duchenne Muscular Dystrophy." University of Southern Queensland, Faculty of Sciences, 2003. http://eprints.usq.edu.au/archive/00001525/.

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The dystrophinopathies are a group of disorders characterised by cellular absence of the membrane stabilising protein, dystrophin. Duchenne muscular dystrophy is the most severe disorder clinically. The deficiency of dystrophin, in the muscular dystrophy X-linked (mdx) mouse causes an elevation in intracellular calcium in cardiac myocytes. Potential mechanisms contributing to increased calcium include enhanced influx, sarcoplasmic reticular calcium release and\or reduced sequestration or sarcolemmal efflux. This dissertation examined the potential mechanisms that may contribute to an intracell

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28

Burt, Matthew. "Resveratrol as a Novel Therapeutic Agent for Treating Duchenne Muscular Dystrophy." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26273.

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Duchenne Muscular Dystrophy (DMD) is an x-linked neuromuscular disease that is caused by an absence of dystrophin protein, rendering skeletal muscle more susceptible to contraction-induced damage. One therapeutic strategy focuses on increasing the expression of endogenous utrophin A, a dystrophin homologue. Interestingly, slow muscle is more resistant to the dystrophic pathology and has increased utrophin A expression (Webster 1998; Gramolini 2001b). These observations led researchers to explore the therapeutic potential of stimulating the slow, oxidative myogenic program (SOMP) in the mdx co

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29

van, Erp Christel. "Modifying function and fibrosis of cardiac and skeletal muscle from mdx mice." University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001521/.

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Duchenne Muscular Dystrophy (DMD) is a fatal condition occurring in approximately 1 in 3500 male births and is due to the lack of a protein called dystrophin. Initially DMD was considered a skeletal myopathy, but the pathology and consequences of cardiomyopathy are being increasingly recognised. Fibrosis, resulting from continual cycles of degeneration of the muscle tissues followed by inadequate regeneration of the muscles, is progressive in both cardiac and skeletal dystrophic muscle. In the heart fibrosis interferes with contractility and rhythm whereas it affects contractile function and c

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30

Ferretti, Renato 1982. "Fatores potencialmente envolvidos na proteção das fibras musculares em músculos intrínsecos da laringe de camundongos mdx." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317583.

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Orientador: Humberto Santo Neto<br>Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-20T21:05:12Z (GMT). No. of bitstreams: 1 Ferretti_Renato_D.pdf: 15919724 bytes, checksum: 2e3e4ba8b562aaaaf3dde85b2e810561 (MD5) Previous issue date: 2012<br>Resumo: Os músculos intrínsecos da laringe (MIL) são protegidos da mionecrose em camundongos mdx, modelo da distrofia muscular de Duchenne (DMD). A DMD caracteriza-se pela mionecrose, causada pela ausência da proteína distrofina (DIS). A DIS se une a um complexo glicoproteínas (CDG), que a

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31

Perronnet, Caroline. "Etude de thérapies génique et pharmacologique visant à restaurer les capacités cognitives d’un modèle murin de la Dystrophie musculaire de Duchenne." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112009.

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L’objectif était d’évaluer l’efficacité de thérapies développées pour traiter la dystrophie musculaire de Duchenne (DMD, due à des mutations du gène de la dystrophine) dans la restauration de déficits cognitifs associés à ce syndrome. Deux pistes thérapeutiques visant à compenser les altérations cérébrales liées à la perte de dystrophine ont été explorées chez les souris mdx, modèle de DMD. Une approche pharmacologique basée sur la surexpression de l’utrophine, homologue de la dystrophine, n’améliore pas les déficits comportementaux des souris mdx. Par contre, une intervention génique basée su

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32

Rivier, François. "Dystrophines et protéines associées : structure, fonction et relation avec la pathologie." Montpellier 1, 1998. http://www.theses.fr/1998MON1T034.

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33

Hnia, Karim. "Interaction Utrophine / bêta-dystroglycan dans le muscle et le système nerveux périphérique de la souris déficiente en dystrophine." Montpellier 1, 2006. http://www.theses.fr/2006MON13508.

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L'analyse des différentes interactions entre les membres du complexe associés à la dystrophine (DGC) a été le centre de plusieurs études biochimiques. Le bêta-dystroglycan prend une place primordiale au sein de ce complexe du fait de son rôle de protéine d'ancrage de la dystrophine et/ou de l'utrophine. De part son homologie structurale avec la dystrophine, l'utrophine est exprimée dans le muscle des patients DMD et de la souris modèle de cette pathologie, la souris mdx. De plus en plus d'observations soulignent l'implication du bêta-dystroglycan dans des évènements de signalisation. Comme l'o

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34

Chevron, Marie-Pierre. "Dystrophine et utrophine dans les dystrophies musculaires et au cours du développemnt des muscles squelettique, cardiaque et lisse humains." Montpellier 1, 1994. http://www.theses.fr/1994MON1T023.

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35

Grunwald, Stefanie. "Identifizierung und Charakterisierung von Muskeldystrophie Duchenne modifizierenden Genen und Stoffwechselwegen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16108.

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Hintergrund und Zielsetzung: DMD ist die häufigste Form der Muskeldystrophie im Kindesalter und bis heute unheilbar. Sie wird durch das Fehlen des Proteins Dystrophin verursacht, welches verschiedene Signaltransduktionswege beeinflusst. Das Anliegen der Arbeit ist die Untersuchung und Modulation von Signaltransduktionswegen, die als alternative Therapiestrategie den Verlust von Dystrophin kompensieren könnten. Experimentelle Strategie: Für die Charakterisierung von Dystrophin nachgeschalteten Prozessen wurden mRNA-Expressionsanalysen in Muskelgeweben von DMD-Patienten und einem DMD-Brüderpaa

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36

Sene, Abdoulaye. "Caractérisation des complexes macromoléculaires Dp71-utrophine/DAPs responsables de l'agrégation des canaux Kir4. 1 at AQP4 dans la cellule gliale de Müller de la rétine : implications fonctionnelles." Paris 6, 2009. http://www.theses.fr/2009PA066225.

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La Dp71, un produit court du gène DMD (Dystrophie Musculaire de Duchenne) est une protéine intracellulaire du cytosquelette associé à la membrane et présentant le même patron d’expression que les canaux potassiques Kir4. 1 et aqueux AQP4 dans la cellule gliale de Müller (CGM) de la rétine. Nous avons identifié le complexe macromoléculaire qui se forme autour de la Dp71 et qui est responsable de la localisation et de l’agrégation des canaux Kir4. 1 et AQP4 dans la CGM. En utilisant la souris Dp71-null, nous avons pu étudier la composition du complexe se formant autour de l’utrophine en absence

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37

Humston, Jill Louise. "Identification and characterization of novel binding partners for dystrophin and utrophin." 2008. http://www.library.wisc.edu/databases/connect/dissertations.html.

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