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Tesis sobre el tema "Dystrophin"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Gaschen, Lorrie. "Cardiomyopathy in dystrophin-deficient hypertrophic feline muscular dystrophy /." [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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2

Howard, Judith. "Electrodiagnostic evaluation of dystrophin-deficient hypertrophic feline muscular dystrophy /." [S.l.] : [s.n.], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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3

Thorley, Matthew. "Analysis of the dystrophin interactome." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066619/document.

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Le but de ce projet était d'identifier de manière méthodique et standardisée les partenaires interagissant avec la protéine dystrophine dans les cellules musculaires squelettiques humaines différenciées et découvrir de nouveaux rôles de la dystrophine. Des cellules immortalisées ont été obtenue en sur-exprimant de manière stable hTERT / CDK4. Nous avons réalisé une analyse transcriptomique comparant des lignées immortalisées avec leurs populations primaires correspondantes, à l’état de prolifération et de différentiation. Nous avons constaté que l'immortalisation n'a pas d'effet mesurable sur

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4

Acharyya, Swarnali. "Elucidating molecular mechanisms of muscle wasting in chronic diseases." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1180096565.

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5

Thorley, Matthew. "Analysis of the dystrophin interactome." Electronic Thesis or Diss., Paris 6, 2016. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2016PA066619.pdf.

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Le but de ce projet était d'identifier de manière méthodique et standardisée les partenaires interagissant avec la protéine dystrophine dans les cellules musculaires squelettiques humaines différenciées et découvrir de nouveaux rôles de la dystrophine. Des cellules immortalisées ont été obtenue en sur-exprimant de manière stable hTERT / CDK4. Nous avons réalisé une analyse transcriptomique comparant des lignées immortalisées avec leurs populations primaires correspondantes, à l’état de prolifération et de différentiation. Nous avons constaté que l'immortalisation n'a pas d'effet mesurable sur

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6

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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7

Coovert, Daniel David. "Analysis of dystrophin in duchenne muscular dystrophy and SMN in spinal muscular atrophy /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487951595500021.

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8

Reza, Mojgan. "Engineering and optimisation of mini-dystrophin constructs for Duchenne muscular dystrophy gene therapy." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2827.

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Muscular dystrophies (MDs) are inherited disorders characterised by muscle weakness and atrophy. One of the most severe forms is Duchenne muscular dystrophy (DMD) which together with the milder allelic form Becker muscular dystrophy (BMD) are known as the dystrophinopathies and result from defects in the X-linked gene encoding dystrophin. Dystrophin is a structural protein of the muscle that connects the internal cytoskeleton of muscle fibres to the extracellular matrix. DMD is also amongst the most common forms of muscular dystrophy, affecting ~1 in 4000 live male birth and manifests as rapid

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9

Johnson, Eric K. "A new model for the dystrophin associated protein complex in striated muscles." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354554580.

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10

Steen, Michelle Sabrina. "Analyses of alpha-dystrobrevin-null mice implicate Niemann-Pick C1 in muscular dystrophy /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/10537.

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11

Howard, Perry Leigh. "The functional diversity of dystrophin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0001/NQ41177.pdf.

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12

Bestard, Jennifer. "Dystrophin gene regulation in muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/MQ54086.pdf.

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13

Ajdukovic, Boris. "Dystrophin expression during skeletal myogenesis." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56988.

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The factors that regulate dystrophin accumulation, and its association with other proteins in culture, are largely unknown. In this study I have examined the effects of chemical agents on dystrophin accumulation in culture, as well as determined whether dystrophin in culture has associations with glycoproteins in a similar fashion to that found in normal muscle tissue. My results show that the onset of detectable dystrophin accumulation occurs shortly after myoblast fusion has taken place, and increases rapidly thereafter as a percentage of total cell protein. The effects of depolarizing conce

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14

Laws, Nicola. "Characterisation and strategic treatment of dystrophic muscle." University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001457/.

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The mdx mouse is widely used as a model for Duchenne Muscular Dystrophy, a fatal X-linked disease caused by a deficiency of the sub-sarcolemmal protein, dystrophin. This dissertation reports characterisation of the features of dystrophy in the mdx mouse, including parameters such as electrophysiological and contractile properties of dystrophic cardiac tissue, quantitative evaluation of kyphosis throughout the mdx lifespan, and contractile properties of respiratory and paraspinal muscles. Following these characterisation studies, the efficacy of antisense oligonucleotides (AOs) to induce altern

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15

Anderson, Jennifer Louise Medical Sciences Faculty of Medicine UNSW. "Cerebellar synaptic plasticity in two animal models of muscular dystrophy." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43524.

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Duchenne muscular dystrophy (DMD) and congenital muscular dystrophy 1A (MDC1A) are the two most common forms of muscular dystrophy in humans, caused by mutations in dystrophin and laminin α2 genes respectively. Both are severe forms of the disease that lead to premature death due and are both now known to have a significant effect on the central nervous system. This project investigated the role of both proteins involved in each of these diseases in cerebellar Purkinje cells of two murine models of disease: the mdx mouse a dystrophin-deficient model of DMD and the dy2J a laminin α2-deficient m

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16

Montanaro, Federica. "The role of dystroglycan in muscular dystrophy and synaptogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ55361.pdf.

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17

Lekan, Jaimy Marie. "Exercise-induced mechanisms of muscle adaptation in mdx mice." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379.

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18

Milad, Nadia. "Effects of hyperlipidemia on dysferlin- and dystrophin-deficient muscular dystrophies in double-disease mouse models." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/60999.

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The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.<br>Medicine, Faculty of<br>Anesthesiology, Pharmacology and Therapeutics, Department of<br>Graduate

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19

England, Sarah Beatrice. "Molecular studies of the dystrophin gene." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257954.

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20

Thanh, Le Thiet. "Exon-specific monoclonal antibodies against dystrophin." Thesis, University of Salford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261661.

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21

SPITALI, Pietro. "ANTISENSE MEDIATED DYSTROPHIN READING FRAME RESTORATION." Doctoral thesis, Università degli studi di Ferrara, 2010. http://hdl.handle.net/11392/2389323.

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Exon skipping using antisense oligonucleotides (AONs) has successfully been used to reframe the mRNA in various DMD (Duchenne muscular dystrophy) patients carrying deletions and in the mdx mouse model. This study can be devided in two parts: in the first part we have tested the feasibility of the exon skipping approach for patients with small mutations in in-frame exons, while in the second part a quantitative comparison of exon skipping revealing techniques is addressed. We first identified 55 novel disease-causing point mutations. We selected 5 patients with nonsense or frameshifting

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22

Betts, Corinne A. "Exon skipping peptide-pmos for correction of dystrophin in mouse models of duchenne muscular dystrophy." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:545d586a-ad7b-4089-8537-b2677957b874.

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Duchenne muscular dystrophy (DMD) is a fatal, muscle-wasting disorder due to mutations/deletions in the dystrophin gene. Whilst improvements in palliative care have increased the life expectancy of patients, cardiomyopathy and respiratory complications are still the leading causes of death. A potential therapy for the treatment of DMD is antisense oligonucleotides (AOs), which modulate dystrophin pre-mRNA splicing to restore the dystrophin reading frame and generate a truncated functional protein. Conjugation of AOs to cell penetrating peptides (CPP), such as Pip5e-, significantly improves del

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23

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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24

Deol, Jatinderpal. "Development of helper-dependent adenovirus for gene expression in muscle." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33745.

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Duchenne muscular dystrophy (DMD) is characterized by necrosis and progressive loss of muscle fibers. DMD patients have a mutation in the gene encoding dystrophin, a large membrane-associated cytoskeletal protein on the cytoplasmic side of the sarcolemma. Gene therapy using fully deleted adenoviral vectors shows great potential for the eventual treatment of DMD and other genetic diseases. These vectors are less immunogenic than their predecessors and have the capacity to carry large DNA inserts such as the full-length dystrophin (12 kb). However, the lack of viral genes results in a weakened a

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25

Judge, Luke Milburn. "Dissecting the signaling and mechanical functions of the dystrophin-glycoprotein complex in skeletal muscle /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/4989.

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26

Dutton, Anna Louise. "An investigation into the effects of dystrophin on the lateral mobility of muscle membrane components." Thesis, Durham University, 1999. http://etheses.dur.ac.uk/4576/.

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Dystrophin is the product of the Duchenne Muscular Dystrophy gene locus, whose absence results in progressive skeletal muscle breakdown. Despite considerable work on the localisation of dystrophin and its associated complex, its role in muscle function remains unclear. In the light of the structural and mechanical instability of the dystrophic membrane, the idea was tested that dystrophin might impart membrane integrity and strength by anchoring membrane proteins and/or delineating the surface into specialised subcellular functional domains. Specifically, because dystrophin shows high sequence

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27

Thorogood, Francesca Clare. "Modulation of dystrophin pre-mRNA splicing by antisense oligonucleotides : a potential therapy for Duchenne muscular dystrophy." Thesis, Royal Holloway, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504809.

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Duchenne muscular dystrophy (DMD) is an X-linked muscle wasting disorder caused by mutations in the gene for dystrophin, a 427kDa cytoskeletal protein important for maintaining the integrity of muscle fibres. A number of DMD mutations result in an absence of functional protein due to disruption of the translational reading frame. It has been shown previously that antisense oligonucleotide (AON) reagents can modulate dystrophin pre-mRNA splicing to specifically exclude an out-of-frame exon from the mRNA. This restores the open reading frame resulting in production of a semi-functional internall

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28

Tandon, Animesh. "Dystrophin genotype-cardiac phenotype correlations in Duchenne and Becker muscular dystrophy using cardiac magnetic resonance imaging." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1396453528.

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29

Thorley, Matthew [Verfasser]. "Analysis of the dystrophin interactome / Matthew Thorley." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/1128646315/34.

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30

Guibinga, Ghiabe H. "Molecular therapeutic interventioan for dystrophin-deficient muscles." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36945.

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Duchenne muscular dystrophy (DMD) is common and fatal X-linked genetic disorder. The overall objective of this thesis was to carry out a prospective study for dystrophin gene therapy in dystrophic muscles, using the X-linked muscular dystrophy (mdx) mouse model. Recombinant adenovirus (AdV) is presently the vehicle of choice for gene therapy for a number of diseases including DMD. However AdV possess two major limitations when utilized as vectors in skeletal muscles: (i) the maturation-dependency of AdV-infectivity in skeletal muscles, (ii) the host immune response against adenoviral proteins

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31

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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32

Cisternas, Felipe A. "The function of alternatively spliced isoforms of dystrophin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ49767.pdf.

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33

Ditta, Stephanie Doreen. "Matrix attachment regions in the human dystrophin gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ53801.pdf.

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34

Demacio, Paula Constance. "Characterization of dystrophin protein complexes in the retina." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63719.pdf.

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35

Geng, Yan. "Molecular genetic studies of the mouse dystrophin gene." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239374.

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36

Loh, Nellie Y. "Characterisation of #beta#-dystrobrevin, a dystrophin-related protein." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299483.

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37

Yazid, Muhammad Da'In Bin. "Analysis of cell signalling in dystrophin-deficient myoblasts." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7342/.

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An absence of dystrophin in muscle has a massive impact throughout muscle development, and Duchene Muscular Dystrophy (DMD) is one of the consequences. The disruption of the dystrophin-glycoprotein complex (DGC) is caused by a mutation in the dmd gene, which effects muscle integrity, resulting in progressive muscle degeneration and weakness. In this study, dfd13 (dystrophin-deficient) and C2C12 (non-dystrophic) myoblasts were cultured in low mitogen conditions for 10 days to induce differentiation; however, dfdl3 myoblasts did not achieve terminal differentiation. It has been suggested that Pa

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38

Li, Hongmei. "Precise Correction of the Dystrophin Gene in Duchenne Muscular Dystrophy Patient iPS Cells by TALEN and CRISPR-Cas9." Kyoto University, 2015. http://hdl.handle.net/2433/199179.

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39

Sako, Yukiya. "Development of an orally available inhibitor of CLK1 for skipping a mutated dystrophin exon in Duchenne muscular dystrophy." Kyoto University, 2017. http://hdl.handle.net/2433/226771.

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40

Thompson, Shannon. "Exploring Dystrophin-Mediated Control of Neural Stem Cell Fate Associated with Intellectual Disability In Duchenne Muscular Dystrophy Patients." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38110.

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Duchenne Muscular Dystrophy (DMD) is an X-linked recessive neuromuscular disease characterized by progressive muscle-wasting and loss of mobility. One-third of patients with DMD are also affected by cognitive impairments such as a lower than average IQ and impaired working memory, comorbid with neuropsychiatric disorders such as anxiety and autism-related behaviours. DMD is caused by mutations in the DMD gene resulting in the deletion of the full-length dystrophin protein (Dp427) and, dependent on mutation, other dystrophin isoforms. These isoforms are predominantly found in the brain and del

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41

Rangan, Apoorva. "CRISPR-Cas9 Mediated Restoration of Dystrophin Expression and Inhibition of Myostatin: A Novel Gene Therapy for Duchenne Muscular Dystrophy." Scholarship @ Claremont, 2016. http://scholarship.claremont.edu/cmc_theses/1305.

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Duchenne Muscular Dystrophy (DMD) is an X-linked recessive genetic disease, caused by a frame-shift mutation in the dystrophin gene. Current gene therapies for DMD target dystrophin transcripts in existing skeletal and cardiac muscle, rather than adipose and fibrotic tissues. These approaches may be unable to repair muscle functionality in DMD patients who have already undergone extensive muscle damage and wasting. Thus, successful DMD therapies must consider the underlying genetic cause and pathology. Inhibition of the gene myostatin, a negative regulator of muscle growth, has been shown to a

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42

Gardner, Katherine Lynn. "New insights into the disease mechanisms of Duchenne Muscular Dystrophy through analyses of the Dystrophin, IκBβ, and CASK proteins". The Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=osu1153530409.

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43

Hance, Jacqueline Elizabeth. "Identification of novel components of the dystrophin glycoprotein complex." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ40057.pdf.

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44

Sommer, Barbara. "Changes of skeletal muscle in adult dystrophin-deficient cats /." [S.l.] : [s.n.], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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45

Oliveira, Daniela Moraes de. "Análise de expressão da distrofina, miostatina, tgf-β e nf-kappa β, durante a fase embrionária e fetal no modelo canino GRMD (Golden Retrivier Muscular Dystrophy)." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-27022018-121625/.

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A Distrofia Muscular de Duchenne (DMD) é uma doença genética neuromuscular hereditária, ligada ao cromossomo X, sendo encontrada em humanos do sexo masculino. Esta doença muscular é descrita em outras espécies. O modelo de estudo pré-clínico GRMD (Golden Retrievier Muscular Dystrophy) apresenta sintomas clínicos fenotipicamente característicos da DMD em humanos e, por esta razão, tem sido amplamente utilizado como modelo de estudos pré-clínicos. O objetivo da presente pesquisa foi avaliar o tecido muscular, no modelo canino distrófico, ao longo da gestação. Quatro fêmeas, portadoras do gene di

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46

Kaspar, Rita Wen. "Genotype-Phenotype Association Analysis of Dilated Cardiomyopathy in Becker Muscular Dystrophy." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243469474.

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47

Palmieri, Laura. "Development of 3D muscle tissues for gene therapy screening and therapeutic evaluation of novel Midi-Dystrophins in Duchenne Muscular Dystrophy context." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL056.

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La dystrophie musculaire de Duchenne (DMD), encore incurable, est due à l'absence de dystrophine, une protéine essentielle pour préserver l'intégrité musculaire continuellement mise à l'épreuve par les contractions. La thérapie génique utilisant le virus adéno-associé (AAV) pour délivrer des formes tronquées de dystrophine (µDys) est actuellement l'approche thérapeutique la plus prometteuse. Cependant, les résultats obtenus chez les patients diffèrent de ceux des études animales, ce qui souligne la nécessité de disposer de modèles permettant de prédire avec précision la réponse humaine. En out

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48

Murphy, Stephen James. "Adenovirus vectors for gene transfer of full-length dystrophin cDNAs." Thesis, Royal Holloway, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300462.

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49

Ferrer, Roig Aurora. "Immune responses to dystrophin : implications for gene therapy of DMD." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395118.

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50

Byth, Barbara Christian. "Molecular analysis of an autosomal homologue of the dystrophin gene." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302841.

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