Relevant bibliographies by topics / Dystrophin

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Academic literature on the topic 'Dystrophin'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 October 2024

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Journal articles on the topic "Dystrophin"

1

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. In contrast, mdx mice, a dystrophin-deficient animal model for Duchenne muscular dystrophy, showed significant Evans blue accumulation in skeletal muscle fibers. We also studied Evans blue dispersion in transgenic mice bearing different dystrophin mutations, and we demonstrated that cytoskeletal and sarcolemmal attachment of dystrophin might be a necessary requirement to prevent serious fiber damage. The extent of dye incorporation in transgenic mice correlated with the phenotypic severity of similar dystrophin mutations in humans. We furthermore assessed Evans blue incorporation in skeletal muscle of the dystrophia muscularis (dy/dy) mouse and its milder allelic variant, the dy2J/dy2J mouse, animal models for congenital muscular dystrophy. Surprisingly, these mice, which have defects in the laminin α2-chain, an extracellular ligand of the DGC, showed little Evans blue accumulation in their skeletal muscles. Taken together, these results suggest that the pathogenic mechanisms in congenital muscular dystrophy are different from those in Duchenne muscular dystrophy, although the primary defects originate in two components associated with the same protein complex.
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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 dystrophied muscle. In vivo transfer of menstrual blood–derived cells into dystrophic muscles of immunodeficient mdx mice restored sarcolemmal expression of dystrophin. Labeling of implanted cells with enhanced green fluorescent protein and differential staining of human and murine nuclei suggest that human dystrophin expression is due to cell fusion between host myocytes and implanted cells. In vitro analysis revealed that endometrial progenitor cells and menstrual blood–derived cells can efficiently transdifferentiate into myoblasts/myocytes, fuse to C2C12 murine myoblasts by in vitro coculturing, and start to express dystrophin after fusion. These results demonstrate that the endometrial progenitor cells and menstrual blood–derived cells can transfer dystrophin into dystrophied myocytes through cell fusion and transdifferentiation in vitro and in vivo.
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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 cause a progressive neurodegenerative, lysosomal storage disorder. Transgenic expression of NPC1 in skeletal muscle ameliorates muscular dystrophy in the Dtna−/− mouse (which has a relatively mild dystrophic phenotype) and in the mdx mouse, a model for DMD. These results identify a new compensatory gene for muscular dystrophy and reveal a potential new therapeutic target for DMD.
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4

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 functionally analogous complex. SSPN directly interacts with the UGC and functions to stabilize utrophin protein without increasing utrophin transcription. These findings reveal the importance of protein stability in the prevention of muscular dystrophy and may impact the future design of therapeutics for muscular dystrophies.
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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. One developmentally regulated gene characterized in detail, α-cardiac actin, showed abnormal persistent expression after birth in 60% of Duchenne dystrophy myofibers. The majority of myofibers (∼80%) remained strongly positive for this protein throughout the course of the disease. Other developmentally regulated genes that showed widespread overexpression in these muscular dystrophies included embryonic myosin heavy chain, versican, acetylcholine receptor α-1, secreted protein, acidic and rich in cysteine/osteonectin, and thrombospondin 4. We hypothesize that the abnormal Ca2+ influx in dystrophin- and α-sarcoglycan–deficient myofibers leads to altered developmental programming of developing and regenerating myofibers. The finding of upregulation of HLA-DR and factor XIIIa led to the novel identification of activated dendritic cell infiltration in dystrophic muscle; these cells mediate immune responses and likely induce microenvironmental changes in muscle. We also document a general metabolic crisis in dystrophic muscle, with large scale downregulation of nuclear-encoded mitochondrial gene expression. Finally, our expression profiling results show that primary genetic defects can be identified by a reduction in the corresponding RNA.
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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 dystrophin, and in particular to the b isoform of dystrophin. These results indicate that dystrophin is a component of the postsynaptic membrane at neuromuscular synapses and raise the possibility that loss of dystrophin from synapses in dystrophic muscle may have consequences that contribute to muscular dystrophy.
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7

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 novel rat model carrying in-frame Dmd gene mutations (IF rats) and evaluated the pathology. We found that IF rats exhibited reduced expression of truncated dystrophin in a proteasome-independent manner. This abnormal dystrophin expression caused dystrophic changes in muscle tissues but did not lead to functional deficiency. We also found that the expression of additional dystrophin named dpX, which forms the DGC in the sarcolemma, was associated with the appearance of truncated dystrophin. In conclusion, the outcomes of this study contribute to the further understanding of BMD pathology and help elucidate the efficiency of dystrophin recovery treatments in Duchenne muscular dystrophy, a more severe form of X-linked muscular dystrophy.
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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 Counter to our hypothesis, markers of autophagy were similar between groups. Given these surprising results, two independent experiments were conducted using 14-month-old mdx mice or 10-month-old mdx/Utrn± mice, a more severe model of Duchenne muscular dystrophy. Data from these animals suggest increased autophagosome degradation. Conclusion Together these data suggest that autophagy is not impaired in the dystrophic myocardium as it is in dystrophic skeletal muscle and that disease progression and related injury is independent of autophagic dysfunction.
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Ibrahim Sory, P., T. Sidi, L. Guida, K. Boureima, M. Alassane Bameye, T. Mohomodine Ibrahim, K. Abdoulaye, and C. Idrissa Ahmadou. "Dystrophie Musculaire de Duchenne: Aspects cliniques, biologiques et évolutifs à propos de cinq cas dans le service de Rhumatologie au CHU du Point G." Rhumatologie Africaine Francophone 6, no. 2 (January 19, 2024): 18–23. http://dx.doi.org/10.62455/raf.v6i2.53.

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Résumé La dystrophie musculaire de Duchenne (DMD) due à la non expression de la dystrophine est liée au chromosome X. Décrite au 19e siècle, est la plus courante dystrophie musculaire de l’enfant [1, 2]. L’incidence est estimée à 30 cas pour 100 000 naissances [1, 2]. But- étudier les caractères cliniques, biologiques et évolutifs de la dystrophie musculaire de Duchenne. Patients et Méthodes : Il s’est agi d’une étude rétrospective portant sur 5 dossiers de DMD, colligés en 7 ans. Résultats Nous rapportons cinq dossiers de garçons colligés entre 2005 et 2012, 2012, d’âge moyen de 7 ans avec des extrêmes de 1 et 12 ans. L’hypertrophie des mollets et la présence d’un signe de Gowers chez 4/5 patients. Le caractère familial était présent chez 2 garçons âgés de 5 et 10 ans à l’inclusion dont un mariage consanguin. L’examen anatomopathologique musculaire a conclu à des lésions dystrophiques. L’immunohistochimie n’a pas trouvé d’expression de la dystrophine. La corticothérapie précocement instituée à 0,5 mg/kg/jour associée à la rééducation kinésithérapie a maintenu l’autonomie des patients. Conclusion La corticothérapie retarderait les complications cardio-pulmonaires. Associée à la rééducation kinésithérapie et aux conseils pratiques elle a diminué les chutes. Mots clés : Dystrophie – Musculaire – Duchenne, Rhumatologie Bamako Abstract: Introduction Duchenne’s muscular dystrophy (DMD) caused by no dystrophin expression is linked to X chromosome. Described in the 19th century, it is the most common muscular dystrophy of the child [1, 2]. The incidence is estimated at 30 cases per 100 000 births [1, 2]. Goal - Study clinical, biological and evolutive aspects of the Duchenne's Muscular Dystrophy. Patients and Methods: It was a retrospective study about 5 cases of DMD, collected in 7 years [2005-2012]. Results During our study from the period of 2005 to 2012, we had 5 cases of boys with an average age of 7 years and the extreme age from 1 year to 12 years. The calf’s hypertrophy and the presence of a Gowers’s sign in 4/5 patients. Family caracteristic was present in two boys aged 5 and 10 years with a consanguineous marriage. Muscular Histological examination concluded dystrophic lesions. The immunohistiochemistry found no expression of dystrophin. Corticosteroids early established at 0.5 mg / kg / day combined with physiotherapy rehabilitation maintained the autonomy of patients. . Conclusion Corticosteroids would slow douwn cardiopulmonary complications. Associated with the physiotherapy rehabilitation and practical advice, it has decreased falls. Keywords: Duchenne’s muscular dystrophy, Rheumatology, Bamako
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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 not completely understood. While abnormally elevated resting cytosolic Ca2+ concentration is found in all dystrophic cells, the aberrant mechanisms leading to that outcome have cell-specific components. We probe the diverse aspects of calcium response in various affected tissues. In skeletal muscles, cardiomyocytes, and neurons, dystrophin appears to serve as a scaffold for proteins engaged in calcium homeostasis, while its interactions with actin cytoskeleton influence endoplasmic reticulum organisation and motility. However, in myoblasts, lymphocytes, endotheliocytes, and mesenchymal and myogenic cells, calcium abnormalities cannot be clearly attributed to the loss of interaction between dystrophin and the calcium toolbox proteins. Nevertheless, DMD gene mutations in these cells lead to significant defects and the calcium anomalies are a symptom of the early developmental phase of this pathology. As the impaired calcium homeostasis appears to underpin multiple DMD abnormalities, understanding this alteration may lead to the development of new therapies. In fact, it appears possible to mitigate the impact of the abnormal calcium homeostasis and the dystrophic phenotype in the total absence of dystrophin. This opens new treatment avenues for this incurable disease.
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Dissertations / Theses on the topic "Dystrophin"

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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 le programme myogénique ou sur tout autre processus cellulaires, et qu'elle avait un effet protecteur contre le processus de sénescence. Les lignées de cellules musculaires humaines constituent donc de bon model in vitro pour l’étude de l’interactome de la dystrophine. Nous avons déterminé l’interactome de la dystrophine en utilisant l’approche proteomique ‘QUICK’. Nous avons identifié 18 nouveaux partenaires directs de la dystrophine, partenaires étant impliqués dans le transport vésiculaire ou étant des protéines d'adhésion. Ces résultats renforcent les données précédemment publiées suggérant un lien entre la dystrophine et le trafic vésiculaire, ainsi que dystrophine et adhesion cellulaire. Ces nouveaux partenaires ont été ajoutés à l’interactome de la dystrophine, interactome accessible sur le Web: sys-myo.rhcloud.com/dystrophin-interactome. Ce site web est dédié à être un outil facile d’utilisation permettant d’explorer et de visualiser l’interactome de la dystrophine du muscle squelettique
The aim of this project was to systematically identify new interaction partners of the dystrophin protein within differentiated human skeletal muscle cells in order to uncover new roles in which dystrophin is involved, and to better understand how the global interactome is affected by the absence of dystrophin. hTERT/cdk4 immortalized myogenic human cell lines represent an important tool for skeletal muscle research however, disruption of the cell cycle has the potential to affect many other cellular processes to which it also linked. A transcriptome-wide analysis of healthy and diseased lines comparing immortalized lines with their parent primary populations in both differentiated and undifferentiated states testing their myogenic character by comparison with non-myogenic cells found that immortalization has no measurable effect on the myogenic cascade or on any other cellular processes, and that it was protective against the senescence. In this context the human muscle cell lines are a good in vitro model to study the dystrophin interactome. We investigated dystrophin’s interactors using the high-sensitivity proteomics ‘QUICK’ approach. We identified 18 new physical interactors of dystrophin which displayed a high proportion of vesicle transport related proteins and adhesion proteins, strengthening the link between dystrophin and these roles. The proteins determined through previously published data together with the newly identified interactors were incorporated into a web-based data exploration tool: sys-myo.rhcloud.com/dystrophin-interactome, intended to provide an easily accessible and informative view of dystrophins interactions in skeletal muscle
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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 le programme myogénique ou sur tout autre processus cellulaires, et qu'elle avait un effet protecteur contre le processus de sénescence. Les lignées de cellules musculaires humaines constituent donc de bon model in vitro pour l’étude de l’interactome de la dystrophine. Nous avons déterminé l’interactome de la dystrophine en utilisant l’approche proteomique ‘QUICK’. Nous avons identifié 18 nouveaux partenaires directs de la dystrophine, partenaires étant impliqués dans le transport vésiculaire ou étant des protéines d'adhésion. Ces résultats renforcent les données précédemment publiées suggérant un lien entre la dystrophine et le trafic vésiculaire, ainsi que dystrophine et adhesion cellulaire. Ces nouveaux partenaires ont été ajoutés à l’interactome de la dystrophine, interactome accessible sur le Web: sys-myo.rhcloud.com/dystrophin-interactome. Ce site web est dédié à être un outil facile d’utilisation permettant d’explorer et de visualiser l’interactome de la dystrophine du muscle squelettique
The aim of this project was to systematically identify new interaction partners of the dystrophin protein within differentiated human skeletal muscle cells in order to uncover new roles in which dystrophin is involved, and to better understand how the global interactome is affected by the absence of dystrophin. hTERT/cdk4 immortalized myogenic human cell lines represent an important tool for skeletal muscle research however, disruption of the cell cycle has the potential to affect many other cellular processes to which it also linked. A transcriptome-wide analysis of healthy and diseased lines comparing immortalized lines with their parent primary populations in both differentiated and undifferentiated states testing their myogenic character by comparison with non-myogenic cells found that immortalization has no measurable effect on the myogenic cascade or on any other cellular processes, and that it was protective against the senescence. In this context the human muscle cell lines are a good in vitro model to study the dystrophin interactome. We investigated dystrophin’s interactors using the high-sensitivity proteomics ‘QUICK’ approach. We identified 18 new physical interactors of dystrophin which displayed a high proportion of vesicle transport related proteins and adhesion proteins, strengthening the link between dystrophin and these roles. The proteins determined through previously published data together with the newly identified interactors were incorporated into a web-based data exploration tool: sys-myo.rhcloud.com/dystrophin-interactome, intended to provide an easily accessible and informative view of dystrophins interactions in skeletal muscle
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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 rapidly progressive muscle degeneration leading to loss of ambulation and death in the second or third decade from respiratory or cardiac failure. Currently, there is no cure for this devastating disease. Clinical management of symptoms and complications is limited to stabilising the condition, slowing deterioration over time and palliative care. Since discovery of the DMD gene in 1986, researchers have dedicated substantial effort into vector technologies, facilitating the use of gene therapy to reintroduce a functional copy of the dystrophin gene into muscle fibres, a potential approach to treat DMD patients. However, this approach poses additional challenges relative to many gene therapy approaches since the full-length dystrophin cDNA is ~14 kb, exceeding the packaging capacity of most viral vectors. A number of large internal in-frame dystrophin deletions have been identified in patients that produce a relatively mild phenotype with later age of onset and a slower rate of disease progression than classical DMD. This observation has inspired the construction of internally truncated, but largely functional versions of dystrophin suitable for gene transfer using viral vectors. So far the most widely used miniaturised dystrophin transgenes have been tested in AAV-mediated gene delivery which has identified several limitations indicating the use of more favourable transgenes that have smaller deletions, yet carrying more functional parts of dystrophin. In this study human mini-dystrophin constructs of 4.3-7.7 kb in size were designed that retain key functional elements of dystrophin molecule and their relative functionality investigated in mdx mice. The ultimate aim of this study is the characterisation and optimisation of these mini-dystrophin constructs for gene delivery studies via viral vectors as a therapeutic tool for treatment of Duchenne muscular dystrophy.
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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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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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Books on the topic "Dystrophin"

1

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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Book chapters on the topic "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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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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Ervasti, James M., and Kevin P. Campbell. "Dystrophin-associated glycoproteins: their possible roles in the pathogenesis of Duchenne muscular dystrophy." In Molecular and Cell Biology of Muscular Dystrophy, 139–66. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1528-5_6.

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Conference papers on the topic "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 more dystrophin-positive fibers were found within the myocardium than in the GN. We hypothesized that the differences in mechanical loading of the two environments influenced the transplantation and explored whether using MDSCs exposed to mechanical stimulation prior to transplantation could improve transplantation. Our study shows increased engraftment into the heart and GN muscle for cells pretreated with mechanical stretch for 24 hours. This increase was significant for transplantation into the heart. These studies have implications in a variety of applications including mechanotransduction, stem cell biology, and Duchenne muscular dystrophy.
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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 quantification of CD31 positive microvessels. This study is important to aid in determining the in vivo environmental factors leading to large graft size which may aid in determining optimum transplantation conditions for muscle repair.
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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 fiber occurs, releasing muscle serum enzymes. Its characteristics are defined by clinical, histological and electromyographic criteria. The symptoms result from the weakness of the skeletal, cardiac and visceral muscles; progressively worsen; histological changes include muscle degeneration and regeneration, without evidence of abnormal storage of any metabolic; the disease is heritable, even without familial reports. Objectives: To compare the evidence and manifestations of DMD in humans in relation to Golden Retriever dogs with muscular dystrophy (GRMD), from breeders from Seattle-USA, named Canil GRMD — Brasil from the Department of Anatomy of the Faculty of Veterinary Medicine and Zootechnics of the Universidade de São Paulo. Conclusion: The model that most resembles humans are dogs, in terms of clinical and pathological aspects of muscular dystrophy. Golden Retriever dogs (GRMD) are genetically homologous to humans, and their histological lesions are identical to patients with DMD. GRMD dogs have been characterized as an ideal model for studies of the pathological and genetic mechanisms of DMD, as well as therapeutic trials.
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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 failure, leading to death. Spirometric parameters such as forced vital capacity (FVC) are used to monitor lung function. Muscle ultrasound has been increasingly used in neuromuscular diseases, being a possible tool for evaluating respiratory muscles individually and a non-invasive method of assessing diaphragm function. Objectives: This study aims to evaluate lung function and respiratory muscles in patients with DMD at different stages of the disease. Methods: This is a prospective observational study with 25 patients with DMD follow-up at the Hospital das Clínicas de São Paulo (HC/FMUSP), with Assessment of diaphragmatic thickness by ultrasonography in DMD patients and correlate with FVC. Results: Diphragmatic thickness significantly decreased with age and with the reduction of the FVC in DMD patients. Some patients had pseudo hypertrophy of the diaphragm but without related reduction in lung function. Conclusion: Ultrasound of respiratory and appendicular muscles can help in the assessment of respiratory function and possible indirect markers of worsening lung function.
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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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Reports on the topic "Dystrophin"

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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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