Bibliografías temáticas / Dystrophin

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Literatura académica sobre el tema "Dystrophin"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 9 de junio de 2025

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Artículos de revistas sobre el tema "Dystrophin"

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Straub, Volker, Jill A. Rafael, Jeffrey S. Chamberlain, and Kevin P. Campbell. "Animal Models for Muscular Dystrophy Show Different Patterns of Sarcolemmal Disruption." Journal of Cell Biology 139, no. 2 (October 20, 1997): 375–85. http://dx.doi.org/10.1083/jcb.139.2.375.

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Genetic defects in a number of components of the dystrophin–glycoprotein complex (DGC) lead to distinct forms of muscular dystrophy. However, little is known about how alterations in the DGC are manifested in the pathophysiology present in dystrophic muscle tissue. One hypothesis is that the DGC protects the sarcolemma from contraction-induced damage. Using tracer molecules, we compared sarcolemmal integrity in animal models for muscular dystrophy and in muscular dystrophy patient samples. Evans blue, a low molecular weight diazo dye, does not cross into skeletal muscle fibers in normal mice.
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Cui, Chang-Hao, Taro Uyama, Kenji Miyado, Masanori Terai, Satoru Kyo, Tohru Kiyono, and Akihiro Umezawa. "Menstrual Blood-derived Cells Confer Human Dystrophin Expression in the Murine Model of Duchenne Muscular Dystrophy via Cell Fusion and Myogenic Transdifferentiation." Molecular Biology of the Cell 18, no. 5 (May 2007): 1586–94. http://dx.doi.org/10.1091/mbc.e06-09-0872.

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Duchenne muscular dystrophy (DMD), the most common lethal genetic disorder in children, is an X-linked recessive muscle disease characterized by the absence of dystrophin at the sarcolemma of muscle fibers. We examined a putative endometrial progenitor obtained from endometrial tissue samples to determine whether these cells repair muscular degeneration in a murine mdx model of DMD. Implanted cells conferred human dystrophin in degenerated muscle of immunodeficient mdx mice. We then examined menstrual blood–derived cells to determine whether primarily cultured nontransformed cells also repair
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Steen, Michelle S., Marvin E. Adams, Yan Tesch, and Stanley C. Froehner. "Amelioration of Muscular Dystrophy by Transgenic Expression of Niemann-Pick C1." Molecular Biology of the Cell 20, no. 1 (January 2009): 146–52. http://dx.doi.org/10.1091/mbc.e08-08-0811.

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Duchenne muscular dystrophy (DMD) and other types of muscular dystrophies are caused by the loss or alteration of different members of the dystrophin protein complex. Understanding the molecular mechanisms by which dystrophin-associated protein abnormalities contribute to the onset of muscular dystrophy may identify new therapeutic approaches to these human disorders. By examining gene expression alterations in mouse skeletal muscle lacking α-dystrobrevin (Dtna−/−), we identified a highly significant reduction of the cholesterol trafficking protein, Niemann-Pick C1 (NPC1). Mutations in NPC1 ca
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Peter, Angela K., Jamie L. Marshall, and Rachelle H. Crosbie. "Sarcospan reduces dystrophic pathology: stabilization of the utrophin–glycoprotein complex." Journal of Cell Biology 183, no. 3 (November 3, 2008): 419–27. http://dx.doi.org/10.1083/jcb.200808027.

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Mutations in the dystrophin gene cause Duchenne muscular dystrophy and result in the loss of dystrophin and the entire dystrophin–glycoprotein complex (DGC) from the sarcolemma. We show that sarcospan (SSPN), a unique tetraspanin-like component of the DGC, ameliorates muscular dystrophy in dystrophin-deficient mdx mice. SSPN stabilizes the sarcolemma by increasing levels of the utrophin–glycoprotein complex (UGC) at the extrasynaptic membrane to compensate for the loss of dystrophin. Utrophin is normally restricted to the neuromuscular junction, where it replaces dystrophin to form a functiona
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Yeadon, J. E., H. Lin, S. M. Dyer, and S. J. Burden. "Dystrophin is a component of the subsynaptic membrane." Journal of Cell Biology 115, no. 4 (November 15, 1991): 1069–76. http://dx.doi.org/10.1083/jcb.115.4.1069.

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A subsynaptic protein of Mr approximately 300 kD is a major component of Torpedo electric organ postsynaptic membranes and copurifies with the AChR and the 43-kD subsynaptic protein. mAbs against this protein react with neuromuscular synapses in higher vertebrates, but not at synapses in dystrophic muscle. The Torpedo 300-kD protein comigrates in SDS-PAGE with murine dystrophin and reacts with antibodies against murine dystrophin. The sequence of a partial cDNA isolated by screening an expression library with mAbs against the Torpedo 300-kD protein shows striking homology to mammalian dystroph
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Chen, Yi-Wen, Po Zhao, Rehannah Borup, and Eric P. Hoffman. "Expression Profiling in the Muscular Dystrophies." Journal of Cell Biology 151, no. 6 (December 11, 2000): 1321–36. http://dx.doi.org/10.1083/jcb.151.6.1321.

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We used expression profiling to define the pathophysiological cascades involved in the progression of two muscular dystrophies with known primary biochemical defects, dystrophin deficiency (Duchenne muscular dystrophy) and α-sarcoglycan deficiency (a dystrophin-associated protein). We employed a novel protocol for expression profiling in human tissues using mixed samples of multiple patients and iterative comparisons of duplicate datasets. We found evidence for both incomplete differentiation of patient muscle, and for dedifferentiation of myofibers to alternative lineages with advancing age.
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Teramoto, Naomi, Hidetoshi Sugihara, Keitaro Yamanouchi, Katsuyuki Nakamura, Koichi Kimura, Tomoko Okano, Takanori Shiga, et al. "Pathological evaluation of rats carrying in-frame mutations in the dystrophin gene: a new model of Becker muscular dystrophy." Disease Models & Mechanisms 13, no. 9 (August 28, 2020): dmm044701. http://dx.doi.org/10.1242/dmm.044701.

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ABSTRACTDystrophin, encoded by the DMD gene on the X chromosome, stabilizes the sarcolemma by linking the actin cytoskeleton with the dystrophin-glycoprotein complex (DGC). In-frame mutations in DMD cause a milder form of X-linked muscular dystrophy, called Becker muscular dystrophy (BMD), characterized by the reduced expression of truncated dystrophin. So far, no animal model with in-frame mutations in Dmd has been established. As a result, the effect of in-frame mutations on the dystrophin expression profile and disease progression of BMD remains unclear. In this study, we established a nove
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Spaulding, HR, C. Ballmann, JC Quindry, MB Hudson, and JT Selsby. "Autophagy in the heart is enhanced and independent of disease progression in mus musculus dystrophinopathy models." JRSM Cardiovascular Disease 8 (January 2019): 204800401987958. http://dx.doi.org/10.1177/2048004019879581.

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Background Duchenne muscular dystrophy is a muscle wasting disease caused by dystrophin gene mutations resulting in dysfunctional dystrophin protein. Autophagy, a proteolytic process, is impaired in dystrophic skeletal muscle though little is known about the effect of dystrophin deficiency on autophagy in cardiac muscle. We hypothesized that with disease progression autophagy would become increasingly dysfunctional based upon indirect autophagic markers. Methods Markers of autophagy were measured by western blot in 7-week-old and 17-month-old control (C57) and dystrophic (mdx) hearts. Results
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Zabłocka, Barbara, Dariusz C. Górecki, and Krzysztof Zabłocki. "Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences." International Journal of Molecular Sciences 22, no. 20 (October 13, 2021): 11040. http://dx.doi.org/10.3390/ijms222011040.

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Duchenne muscular dystrophy (DMD) leads to disability and death in young men. This disease is caused by mutations in the DMD gene encoding diverse isoforms of dystrophin. Loss of full-length dystrophins is both necessary and sufficient for causing degeneration and wasting of striated muscles, neuropsychological impairment, and bone deformities. Among this spectrum of defects, abnormalities of calcium homeostasis are the common dystrophic feature. Given the fundamental role of Ca2+ in all cells, this biochemical alteration might be underlying all the DMD abnormalities. However, its mechanism is
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Zabłocka, Barbara, Dariusz C. Górecki, and Krzysztof Zabłocki. "Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences." International Journal of Molecular Sciences 22, no. 20 (October 13, 2021): 11040. http://dx.doi.org/10.3390/ijms222011040.

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Duchenne muscular dystrophy (DMD) leads to disability and death in young men. This disease is caused by mutations in the DMD gene encoding diverse isoforms of dystrophin. Loss of full-length dystrophins is both necessary and sufficient for causing degeneration and wasting of striated muscles, neuropsychological impairment, and bone deformities. Among this spectrum of defects, abnormalities of calcium homeostasis are the common dystrophic feature. Given the fundamental role of Ca2+ in all cells, this biochemical alteration might be underlying all the DMD abnormalities. However, its mechanism is
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Tesis sobre el tema "Dystrophin"

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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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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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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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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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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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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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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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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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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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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Libros sobre el tema "Dystrophin"

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J, Winder Steve, ed. Molecular mechanisms of muscular dystrophies. Georgetown, Tex: Landes Bioscience : Eurekah.com, 2006.

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1958-, Brown Susan C., and Lucy Jack A. 1929-, eds. Dystrophin: Gene, protein, and cell biology. Cambridge, U.K: Cambridge University Press, 1997.

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D'Souza, Vinita N. Dystrophin expression in the retina. Ottawa: National Library of Canada, 1995.

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Bestard, Jennifer. Dystrophin gene regulation in muscle. Ottawa: National Library of Canada, 2000.

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Thanh, Le Thiet. Exon-specific monoclonal antibodies against dystrophin. Salford: University of Salford, 1995.

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Dally, Ghassan Y. Characterization of nommuscle isoforms of dystrophin. Ottawa: National Library of Canada, 1996.

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Cisternas, Felipe A. The function of alternatively spliced isoforms of dystrophin. Ottawa: National Library of Canada, 2000.

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1932-, Kakulas Byron A., Howell J. McC, and Roses Allen D, eds. Duchenne muscular dystrophy: Animal models and genetic manipulation. New York: Raven Press, 1992.

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Emery, Alan E. H. Muscular dystrophy, the facts. 2nd ed. Oxford: Oxford University Press, 2000.

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Emery, Alan E. H. Muscular dystrophy. 3rd ed. Oxford: Oxford University Press Inc., 2008.

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Capítulos de libros sobre el tema "Dystrophin"

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Lu-Nguyen, Ngoc, Alberto Malerba, and Linda Popplewell. "Use of Small Animal Models for Duchenne and Parameters to Assess Efficiency upon Antisense Treatment." In Methods in Molecular Biology, 301–13. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_20.

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AbstractDuchenne muscular dystrophy (DMD) is a rare genetic disease affecting 1 in 5000 newborn boys. It is caused by mutations in the DMD gene with a consequent lack of dystrophin protein that leads to deterioration of myofibers and their replacement with fibro-adipogenic tissue. Using antisense oligonucleotides (AONs) to modify out-of-frame mutations in the DMD gene, named exon skipping, is currently considered among the most promising treatments for DMD patients. The development of this strategy is rapidly moving forward, and AONs designed to skip exons 51 and 53 have received accelerated approval in the USA. In preclinical setting, the mdx mouse model, carrying a point mutation in exon 23 of the murine Dmd gene that prevents production of dystrophin protein, has emerged as a valuable tool, and it is widely used to study in vivo therapeutic approaches for DMD. Here we describe the methodology for intravenous delivery of AONs targeting dystrophin through tail vein of mdx mice. Furthermore, the most relevant functional analyses to be performed in living mice, and the most informative histopathological and molecular assays to evaluate the effect of this treatment are detailed.
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Agarwal, Aishwarya, Kunal Verma, Shivani Tyagi, Khushi Gupta, Satish Kumar Gupta, Shrestha Sharma, and Shobhit Kumar. "Muscular Dystrophy: Mutations in the Dystrophin Gene." In Mechanism and Genetic Susceptibility of Neurological Disorders, 341–57. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-9404-5_15.

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Dickson, George, and Matthew Dunckley. "Human dystrophin gene transfer: genetic correction of dystrophin deficiency." In Molecular and Cell Biology of Muscular Dystrophy, 283–302. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1528-5_11.

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Blake, Derek J., and Kay E. Davies. "Dystrophin and the molecular genetics of muscular dystrophy." In Protein Dysfunction in Human Genetic Disease, 219–41. London: Garland Science, 2024. http://dx.doi.org/10.1201/9781003579953-12.

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Mirza, Zeenat, and Sajjad Karim. "Decoding Dystrophin Gene Mutations: Unraveling the Mysteries of Muscular Dystrophy." In Mechanism and Genetic Susceptibility of Neurological Disorders, 75–90. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-9404-5_4.

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Goossens, Remko, and Annemieke Aartsma-Rus. "In Vitro Delivery of PMOs in Myoblasts by Electroporation." In Methods in Molecular Biology, 191–205. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_12.

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AbstractAntisense oligonucleotides (AONs) are small synthetic molecules of therapeutic interest for a variety of human disease. Their ability to bind mRNA and affect its splicing gives AONs potential use for exon skipping therapies aimed at restoring the dystrophin transcript reading frame for Duchenne muscular dystrophy (DMD) patients. The neutrally charged phosphorodiamidate morpholino oligomers (PMOs) are a stable and relatively nontoxic AON modification. To assess exon skipping efficiency in vitro, it is important to deliver them to target cells. Here, we describe a method for the delivery of PMOs to myoblasts by electroporation. The described protocol for the Amaxa 4D X unit nucleofector system allows efficient processing of 16 samples in one nucleocuvette strip, aiding in high-throughput PMO efficacy screens.
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Barresi, Rita, and Susan C. Brown. "Dystrophin and Its Associated Glycoprotein Complex." In Muscle Disease, 95–101. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118635469.ch8.

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Shah, Md Nur Ahad, and Toshifumi Yokota. "Restoring Dystrophin Expression by Skipping Exons 6 and 8 in Neonatal Dystrophic Dogs." In Methods in Molecular Biology, 107–24. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2772-3_6.

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Murphy, Sandra, and Kay Ohlendieck. "Proteomic Profiling of the Dystrophin-Deficient Brain." In Methods in Molecular Biology, 91–105. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7374-3_7.

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López-Martínez, Andrea, Patricia Soblechero-Martín, and Virginia Arechavala-Gomeza. "Evaluation of Exon Skipping and Dystrophin Restoration in In Vitro Models of Duchenne Muscular Dystrophy." In Methods in Molecular Biology, 217–33. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_14.

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AbstractSeveral exon skipping antisense oligonucleotides (eteplirsen, golodirsen, viltolarsen, and casimersen) have been approved for the treatment of Duchenne muscular dystrophy, but many more are in development targeting an array of different DMD exons. Preclinical screening of the new oligonucleotide sequences is routinely performed using patient-derived cell cultures, and evaluation of their efficacy may be performed at RNA and/or protein level. While several methods to assess exon skipping and dystrophin expression in cell culture have been developed, the choice of methodology often depends on the availability of specific research equipment.In this chapter, we describe and indicate the relevant bibliography of all the methods that may be used in this evaluation and describe in detail the protocols routinely followed at our institution, one to evaluate the efficacy of skipping at RNA level (nested PCR) and the other the restoration of protein expression (myoblot), which provide good results using equipment largely available to most research laboratories.
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Actas de conferencias sobre el tema "Dystrophin"

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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly
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Cassino, Theresa R., Masaho Okada, Lauren M. Drowley, Joseph Feduska, Johnny Huard, and Philip R. LeDuc. "Using Mechanical Environment to Enhance Stem Cell Transplantation in Muscle Regeneration." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176545.

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Muscle-derived stem cell (MDSC) transplantation has shown potential as a therapy for cardiac and skeletal muscle dysfunction in diseases such as Duchenne muscular dystrophy (DMD). In this study we explore mechanical environment and its effects on MDSCs engraftment into cardiac and skeletal muscle in mdx mice and neoangiogenesis within the engraftment area. We first looked at transplantation of the same number of MDSCs into the heart and gastrocnemius (GN) muscle of dystrophic mice and the resulting dystrophin expression. We then explored neoangiogenesis within the engraftments through quantifi
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Oliveira, Marco Antônio Rodrigues Gomes de, and Isaura Maria Mesquita Prado. "Evidence and affects in Duchenne muscular dystrophy in children and Golden Retriever dogs." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.302.

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Introduction: Progressive muscular dystrophies differ in different ways due to their age of manifestation, the distribution of muscle weakness and the association of heart, central nervous system and peripheral nervous system. The most severe and common form of muscular dystrophies is Duchenne muscular dystrophy (DMD). Its involvement is 1/3500 male babies born alive and is attributed to 80% of cases of dystrophinopathies. The impairment of the dystrophin-glycoprotein complex in Becker and Duchenne dystrophies, in most congenital and girdle dystrophies, destruction of the sarcolemmal muscle fi
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de Feraudy, Yvan, Rabah Yaou, Karim Wahbi, France Leturcq, and Helge Amthor. "Residual Very Low Dystrophin Levels Mitigate Dystrophinopathy towards Becker’s Muscular Dystrophy." In Abstracts of the 47th Annual Meeting of the SENP (Société Européenne De Neurologie Pédiatrique). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685441.

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Hilton, S., M. Christen, T. Bilzer, K. Matiasek, V. Jagannathan, T. Leeb, and U. Giger. "Dystrophin (DMD) missense variant in cats with Becker type muscular dystrophy." In 31. Jahrestagung der FG „Innere Medizin und klinische Labordiagnostik“ der DVG (InnLab) – Teil 1: Vorträge. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1760811.

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Lima, Karlla Danielle Ferreira, Pedro Henrique Marte Arruda Sampaio, Marco Antonio Veloso Albuquerque, and Edmar Zanoteli. "Evaluation of lung function and respiratory muscles in Duchenne muscular dystrophy." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.695.

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Introduction: Duchenne muscular Dystrophy (DMD) is a genetic disease of recessive inheritance linked to the X chromosome, caused by a mutation in the dystrophin gene. This mutation will result in absence of the dystrophin protein, leading to the degeneration of muscle skeletal. The disease is the most common childhood-onset form of muscular dystrophy and affects males almost exclusively. DMD symptoms onset occurs in early childhood, usually between the ages of three and five years, with progressive muscle weakness and loss of gait in adolescence, progressive cardiomyopathy, and respiratory fai
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Marin, Marija. "Immunogold localization of dystrophin in the erythrocytes of patients with Duchenne-Becker muscular dystrophy." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.373.

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Krause, C., S. Kranig, J. Pöschl, and H. Hudalla. "Frühe T-Zell Immundysregulation im Dystrophin defizienten Tiermodell." In 30. Kongress der Deutschen Gesellschaft für Perinatale Medizin – „Wandel als Herausforderung“. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1739718.

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Franzmeier, Sophie, Jan Stöckl, Shounak Chakraborty, Thomas Fröhlich, Nicole Pfarr, Eckhard Wolf, Jürgen Schlegel, and Kaspar Matiasek. "Complementary transcriptome and proteome analysis of dystrophin-deficient satellite cells." In 67. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1787318.

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Franzmeier, Sophie, Jan Stöckl, Shounak Chakraborty, Thomas Fröhlich, Nicole Pfarr, Eckhard Wolf, Jürgen Schlegel, and Kaspar Matiasek. "Complementary transcriptome and proteome analysis of dystrophin-deficient satellite cells." In 67. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1787366.

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Informes sobre el tema "Dystrophin"

1

Cox, Gregory A. Translational Research for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada609750.

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Cox, Gregory A. Translational Research for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada564543.

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Huard, Johnny, Eric Hoffman, John Day, Kevin Campbell, Xiao Xiao, and Paula Clemens. New Advanced Technology for Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada536121.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas From Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada463709.

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Cnaan, Avital. CINRG: Infrastructure for Clinical Trials in Duchenne Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567633.

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Cnaan, Avital. CINRG: Infrastructure for Clinical Trials in Duchenne Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599521.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas Derived from Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada446877.

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Mahoney, My G., Ulrich Rodeck, and Jouni Uitto. Molecular Characterization of Squamous Cell Carcinomas Derived From Recessive Dystrophic Epidermolysis Bullosa. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada419358.

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Muzafirovic, Armin. Muscular Dystrophy: Lifestyle Strategies to Improve Quality of Life. Ames (Iowa): Iowa State University, December 2023. http://dx.doi.org/10.31274/cc-20240624-1034.

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Martin, Paul T. Translational Studies of GALGT2 Gene Therapy for Duchenne Muscular Dystrophy. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613577.

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