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Articles de revues sur le sujet « Β-sarcoglycan »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Chan, Yiu-mo, Carsten G. Bönnemann, Hart G. W. Lidov, and Louis M. Kunkel. "Molecular Organization of Sarcoglycan Complex in Mouse Myotubes in Culture." Journal of Cell Biology 143, no. 7 (1998): 2033–44. http://dx.doi.org/10.1083/jcb.143.7.2033.

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The sarcoglycans are a complex of four transmembrane proteins (α, β, γ, and δ) which are primarily expressed in skeletal muscle and are closely associated with dystrophin and the dystroglycans in the muscle membrane. Mutations in the sarcoglycans are responsible for four autosomal recessive forms of muscular dystrophy. The function and the organization of the sarcoglycan complex are unknown. We have used coimmunoprecipitation and in vivo cross-linking techniques to analyze the sarcoglycan complex in cultured mouse myotubes. We demonstrate that the interaction between β- and δ-sarcoglycan is re

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Anastasi, Giuseppe, Giuseppina Cutroneo, Antonina Sidoti, et al. "Sarcoglycan Subcomplex Expression in Normal Human Smooth Muscle." Journal of Histochemistry & Cytochemistry 55, no. 8 (2007): 831–43. http://dx.doi.org/10.1369/jhc.6a7145.2007.

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The sarcoglycan complex (SGC) is a multimember transmembrane complex interacting with other members of the dystrophin–glycoprotein complex (DGC) to provide a mechanosignaling connection from the cytoskeleton to the extracellular matrix. The SGC consists of four proteins (α, β, γ, and δ). A fifth sarcoglycan subunit, ∊-sarcoglycan, shows a wider tissue distribution. Recently, a novel sarcoglycan, the ζ-sarcoglycan, has been identified. All reports about the structure of SGC showed a common assumption of a tetrameric arrangement of sarcoglycans. Addressing this issue, our immunofluorescence and

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Hack, Andrew A., Chantal T. Ly, Fang Jiang та ін. "γ-Sarcoglycan Deficiency Leads to Muscle Membrane Defects and Apoptosis Independent of Dystrophin". Journal of Cell Biology 142, № 5 (1998): 1279–87. http://dx.doi.org/10.1083/jcb.142.5.1279.

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γ-Sarcoglycan is a transmembrane, dystrophin-associated protein expressed in skeletal and cardiac muscle. The murine γ-sarcoglycan gene was disrupted using homologous recombination. Mice lacking γ-sarcoglycan showed pronounced dystrophic muscle changes in early life. By 20 wk of age, these mice developed cardiomyopathy and died prematurely. The loss of γ-sarcoglycan produced secondary reduction of β- and δ-sarcoglycan with partial retention of α- and ε-sarcoglycan, suggesting that β-, γ-, and δ-sarcoglycan function as a unit. Importantly, mice lacking γ-sarco- glycan showed normal dystrophin c

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Bouillon, Juliette, Suzanne M. Taylor, Cheryl Vargo, et al. "Beta-sarcoglycan-deficient muscular dystrophy presenting as chronic bronchopneumonia in a young cat." Journal of Feline Medicine and Surgery Open Reports 5, no. 2 (2019): 205511691985645. http://dx.doi.org/10.1177/2055116919856457.

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Case summaryA 5-month-old cat was evaluated for a 3 week history of cough, nasal discharge, decreased appetite and weight loss. Musculoskeletal examination was normal and serum creatine kinase (CK) activity was within the reference interval. The cat was treated during the next 10 months for chronic, persistent pneumonia. Weakness then became apparent, the cat developed dysphagia and was euthanized. Post-mortem evaluation revealed chronic aspiration pneumonia and muscular dystrophy associated with beta (β)-sarcoglycan deficiency.Relevance and novel informationThis is the first report of a cat w

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Bönnemann, Carsten G., Raju Modi, Satoru Noguchi та ін. "β–sarcoglycan (A3b) mutations cause autosomal recessive muscular dystrophy with loss of the sarcoglycan complex". Nature Genetics 11, № 3 (1995): 266–73. http://dx.doi.org/10.1038/ng1195-266.

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Watchko, Jon F., Terrence L. O'Day, and Eric P. Hoffman. "Functional characteristics of dystrophic skeletal muscle: insights from animal models." Journal of Applied Physiology 93, no. 2 (2002): 407–17. http://dx.doi.org/10.1152/japplphysiol.01242.2001.

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Muscular dystrophies are a clinically and genetically heterogeneous group of disorders that show myofiber degeneration and regeneration. Identification of animal models of muscular dystrophy has been instrumental in research on the pathogenesis, pathophysiology, and treatment of these disorders. We review our understanding of the functional status of dystrophic skeletal muscle from selected animal models with a focus on 1) the mdx mouse model of Duchenne muscular dystrophy, 2) the Bio 14.6 δ-sarcoglycan-deficient hamster model of limb-girdle muscular dystrophy, and 3) transgenic null mutant mu

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Scano, Martina, Alberto Benetollo, Francesco Dalla Barba, et al. "Efficacy of Cystic Fibrosis Transmembrane Regulator Corrector C17 in Beta-Sarcoglycanopathy—Assessment of Patient’s Primary Myotubes." International Journal of Molecular Sciences 25, no. 24 (2024): 13313. https://doi.org/10.3390/ijms252413313.

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Limb–girdle muscular dystrophy type 2E/R4 (LGMD2E/R4) is a rare disease that currently has no cure. It is caused by defects in the SGCB gene, mainly missense mutations, which cause the impairment of the sarcoglycan complex, membrane fragility, and progressive muscle degeneration. Here, we studied the fate of some β-sarcoglycan (β-SG) missense mutants, confirming that, like α-SG missense mutants, they are targeted for degradation through the ubiquitin–proteasome system. These data, collected using HEK-293 cells expressing either the I119F- or Y184C mutants of β-SG, were subsequently confirmed i

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Wang, Ruibo, Maria L. Urso, Edward J. Zambraski, Erik P. Rader, Kevin P. Campbell, and Bruce T. Liang. "Adenosine A3 receptor stimulation induces protection of skeletal muscle from eccentric exercise-mediated injury." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 1 (2010): R259—R267. http://dx.doi.org/10.1152/ajpregu.00060.2010.

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Effective therapy to reduce skeletal muscle injury associated with severe or eccentric exercise is needed. The purpose of this study was to determine whether adenosine receptor stimulation can mediate protection from eccentric exercise-induced muscle injury. Downhill treadmill exercise (−15°) was used to induce eccentric exercise-mediated skeletal muscle injury. Experiments were conducted in both normal wild-type (WT) mice and also in β-sarcoglycan knockout dystrophic mice, animals that show an exaggerated muscle damage with the stress of exercise. In the vehicle-treated WT animals, eccentric

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Salvadori, C., G. Vattemi, R. Lombardo, M. Marini, C. Cantile та G. D. Shelton. "Muscular Dystrophy with Reduced β-Sarcoglycan in a Cat". Journal of Comparative Pathology 140, № 4 (2009): 278–82. http://dx.doi.org/10.1016/j.jcpa.2008.12.003.

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Camps, Jordi, Hanne Grosemans, Rik Gijsbers, Christa Maes, and Maurilio Sampaolesi. "Growth Factor Screening in Dystrophic Muscles Reveals PDGFB/PDGFRB-Mediated Migration of Interstitial Stem Cells." International Journal of Molecular Sciences 20, no. 5 (2019): 1118. http://dx.doi.org/10.3390/ijms20051118.

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Progressive muscle degeneration followed by dilated cardiomyopathy is a hallmark of muscular dystrophy. Stem cell therapy is suggested to replace diseased myofibers by healthy myofibers, although so far, we are faced by low efficiencies of migration and engraftment of stem cells. Chemokines are signalling proteins guiding cell migration and have been shown to tightly regulate muscle tissue repair. We sought to determine which chemokines are expressed in dystrophic muscles undergoing tissue remodelling. Therefore, we analysed the expression of chemokines and chemokine receptors in skeletal and

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Hashimoto, Reina, та Masamitsu Yamaguchi. "Genetic link between β-sarcoglycan and the Egfr signaling pathway". Biochemical and Biophysical Research Communications 348, № 1 (2006): 212–21. http://dx.doi.org/10.1016/j.bbrc.2006.07.045.

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Fanin, M., та C. Angelini. "Defective assembly of sarcoglycan complex in patients with β-sarcoglycan gene mutations. Study of aneural and innervated cultured myotubes". Neuropathology and Applied Neurobiology 28, № 3 (2002): 190–99. http://dx.doi.org/10.1046/j.1365-2990.2002.00389.x.

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Barresi, Rita, Valeria Confalonieri, Massimo Lanfossi та ін. "Concomitant deficiency of β- and γ-sarcoglycans in 20 α-sarcoglycan (adhalin)-deficient patients: immunohistochemical analysis and clinical aspects". Acta Neuropathologica 94, № 1 (1997): 28–35. http://dx.doi.org/10.1007/s004010050668.

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Diniz, G., H. Tekgul, F. Hazan, K. Yararbas, and A. Tukun. "Sarcolemmal deficiency of sarcoglycan complex in an 18-month-old Turkish boy with a large deletion in the beta sarcoglycan gene." Balkan Journal of Medical Genetics 18, no. 2 (2015): 71–76. http://dx.doi.org/10.1515/bjmg-2015-0088.

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Abstract Limb-girdle muscular dystrophy type 2E (LGMD-2E) is caused by autosomal recessive defects in the beta sarcoglycan (SGCB) gene located on chromosome 4q12. In this case report, the clinical findings, histopathological features and molecular genetic data in a boy with β sarcoglycanopathy are presented. An 18-month-old boy had a very high serum creatinine phosphokinase (CPK) level that was accidentally determined. The results of molecular analyses for the dystrophin gene was found to be normal. He underwent a muscle biopsy which showed dystrophic features. Immunohistochemistry showed that

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15

Murugesan, Vignesh, Eva Degerman, Ann-Kristin Holmen-Pålbrink та ін. "β-Sarcoglycan Deficiency Reduces Atherosclerotic Plaque Development in ApoE-Null Mice". Journal of Vascular Research 54, № 4 (2017): 235–45. http://dx.doi.org/10.1159/000478014.

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Pegoraro, Elena, Marina Fanin, Corrado Angelini та Eric P. Hoffman. "Prenatal diagnosis in a family affected with β-sarcoglycan muscular dystrophy". Neuromuscular Disorders 9, № 5 (1999): 323–25. http://dx.doi.org/10.1016/s0960-8966(99)00020-6.

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Pozsgai, E. R., D. A. Griffin, K. N. Heller, J. R. Mendell та L. R. Rodino-Klapac. "β-Sarcoglycan gene transfer decreases fibrosis and restores force in LGMD2E mice". Gene Therapy 23, № 1 (2015): 57–66. http://dx.doi.org/10.1038/gt.2015.80.

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18

Perez-Ortiz, Andric C., Martha J. Peralta-Ildefonso, Esmeralda Lira-Romero, et al. "Lack of Delta-Sarcoglycan (Sgcd) Results in Retinal Degeneration." International Journal of Molecular Sciences 20, no. 21 (2019): 5480. http://dx.doi.org/10.3390/ijms20215480.

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Age-related macular degeneration (AMD) is the leading cause of central vision loss and severe blindness among the elderly population. Recently, we reported on the association of the SGCD gene (encoding for δ-sarcoglycan) polymorphisms with AMD. However, the functional consequence of Sgcd alterations in retinal degeneration is not known. Herein, we characterized changes in the retina of the Sgcd knocked-out mouse (KO, Sgcd−/−). At baseline, we analyzed the retina structure of three-month-old wild-type (WT, Sgcd+/+) and Sgcd−/− mice by hematoxylin and eosin (H&E) staining, assessed the Sgcd–

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19

Lim, Leland E., Franck Duclos, Odile Broux та ін. "β–sarcoglycan: characterization and role in limb–girdle muscular dystrophy linked to 4q12". Nature Genetics 11, № 3 (1995): 257–65. http://dx.doi.org/10.1038/ng1195-257.

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Broux, O., F. Duclos, L. E. Lim та ін. "β-sarcoglycan : Characterization and role in limb-girdle muscular dystrophy linked to 4q12". Neuromuscular Disorders 6, № 2 (1996): S9. http://dx.doi.org/10.1016/0960-8966(96)88965-6.

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Dalla Barba, Francesco, Michela Soardi, Leila Mouhib, et al. "Modeling Sarcoglycanopathy in Danio rerio." International Journal of Molecular Sciences 24, no. 16 (2023): 12707. http://dx.doi.org/10.3390/ijms241612707.

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Sarcoglycanopathies, also known as limb girdle muscular dystrophy 3-6, are rare muscular dystrophies characterized, although heterogeneous, by high disability, with patients often wheelchair-bound by late adolescence and frequently developing respiratory and cardiac problems. These diseases are currently incurable, emphasizing the importance of effective treatment strategies and the necessity of animal models for drug screening and therapeutic verification. Using the CRISPR/Cas9 genome editing technique, we generated and characterized δ-sarcoglycan and β-sarcoglycan knockout zebrafish lines, w

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Sharma, Pawan, Aruni Jha, Gerald L. Stelmack та ін. "Characterization of the dystrophin–glycoprotein complex in airway smooth muscle: role of δ-sarcoglycan in airway responsiveness". Canadian Journal of Physiology and Pharmacology 93, № 3 (2015): 195–202. http://dx.doi.org/10.1139/cjpp-2014-0389.

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The dystrophin–glycoprotein complex (DGC) is an integral part of caveolae microdomains, and its interaction with caveolin-1 is essential for the phenotype and functional properties of airway smooth muscle (ASM). The sarcoglycan complex provides stability to the dystroglycan complex, but its role in ASM contraction and lung physiology in not understood. We tested whether δ-sarcoglycan (δ-SG), through its interaction with the DGC, is a determinant of ASM contraction ex vivo and airway mechanics in vivo. We measured methacholine (MCh)-induced isometric contraction and airway mechanics in δ-SG KO

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Gastaldello, Stefano, Simona D'Angelo, Susanna Franzoso та ін. "Inhibition of Proteasome Activity Promotes the Correct Localization of Disease-Causing α-Sarcoglycan Mutants in HEK-293 Cells Constitutively Expressing β-, γ-, and δ-Sarcoglycan". American Journal of Pathology 173, № 1 (2008): 170–81. http://dx.doi.org/10.2353/ajpath.2008.071146.

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Hashimoto, Reina, та Masamitsu Yamaguchi. "Dynamic Changes in the Subcellular Localization of Drosophila β-Sarcoglycan during the Cell Cycle". Cell Structure and Function 31, № 2 (2006): 173–80. http://dx.doi.org/10.1247/csf.06025.

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Sewry, C. A., J. Taylor, L. V. B. Anderson та ін. "Abnormalities in α-, β- and γ-sarcoglycan in patients with limb-girdle muscular dystrophy". Neuromuscular Disorders 6, № 6 (1996): 467–74. http://dx.doi.org/10.1016/s0960-8966(96)00389-6.

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Bönnemann, C., J. Wong, C. Ben Hamida, M. Ben Hamida, F. Hentati та L. Kunkel. "LGMD 2E in Tunisia is caused by a missense mutation Arg91Leu in β-sarcoglycan". Neuromuscular Disorders 7, № 6-7 (1997): 460. http://dx.doi.org/10.1016/s0960-8966(97)87298-7.

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Draviam, Romesh A., Stuart H. Shand та Simon C. Watkins. "The β-δ-core of sarcoglycan is essential for deposition at the plasma membrane". Muscle & Nerve 34, № 6 (2006): 691–701. http://dx.doi.org/10.1002/mus.20640.

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Chockalingam, Priya Sethu, Rushina Cholera, Shilpa A. Oak, Yi Zheng, Harry W. Jarrett, and Donald B. Thomason. "Dystrophin-glycoprotein complex and Ras and Rho GTPase signaling are altered in muscle atrophy." American Journal of Physiology-Cell Physiology 283, no. 2 (2002): C500—C511. http://dx.doi.org/10.1152/ajpcell.00529.2001.

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The dystrophin-glycoprotein complex (DGC) is a sarcolemmal complex whose defects cause muscular dystrophies. The normal function of this complex is not clear. We have proposed that this is a signal transduction complex, signaling normal interactions with matrix laminin, and that the response is normal growth and homeostasis. If so, the complex and its signaling should be altered in other physiological states such as atrophy. The amount of some of the DGC proteins, including dystrophin, β-dystroglycan, and α-sarcoglycan, is reduced significantly in rat skeletal muscle atrophy induced by tenotom

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Bauer, Ralf, Alison Blain, Elizabeth Greally та ін. "Intolerance to β-blockade in a mouse model of δ-sarcoglycan-deficient muscular dystrophy cardiomyopathy". European Journal of Heart Failure 12, № 11 (2010): 1163–70. http://dx.doi.org/10.1093/eurjhf/hfq129.

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Beckmann, J. S., I. Richard, O. Broux та ін. "Identification of muscle-specific calpain and β-sarcoglycan genes in progressive autosomal recessive muscular dystrophies". Neuromuscular Disorders 6, № 6 (1996): 455–62. http://dx.doi.org/10.1016/s0960-8966(96)00386-0.

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Beckmann, J. S., I. Richard, O. Broux та ін. "Identification of muscle-specific calpain and β-sarcoglycan genes in progressive autosomal recessive muscular dystrophies". Neuromuscular Disorders 6, № 2 (1996): S7. http://dx.doi.org/10.1016/0960-8966(96)88956-5.

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Andersson, Daniel C., Albano C. Meli, Steven Reiken та ін. "Leaky ryanodine receptors in β-sarcoglycan deficient mice: a potential common defect in muscular dystrophy". Skeletal Muscle 2, № 1 (2012): 9. http://dx.doi.org/10.1186/2044-5040-2-9.

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Duclos, F., O. Broux, N. Bourg та ін. "β-Sarcoglycan: genomic analysis and identification of a novel missense mutation in the LGMD2E Amish isolate". Neuromuscular Disorders 8, № 1 (1998): 30–38. http://dx.doi.org/10.1016/s0960-8966(97)00135-1.

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Bönnemann, C. G., J. Wong, Ch Ben Hamida, M. Ben Hamida, F. Hentati та L. M. Kunkel. "LGMD 2E in Tunisia is caused by a homozygous missense mutation in β-sarcoglycan exon 3". Neuromuscular Disorders 8, № 3-4 (1998): 193–97. http://dx.doi.org/10.1016/s0960-8966(98)00014-5.

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Durbeej, Madeleine, Ronald D. Cohn, Ronald F. Hrstka та ін. "Disruption of the β-Sarcoglycan Gene Reveals Pathogenetic Complexity of Limb-Girdle Muscular Dystrophy Type 2E". Molecular Cell 5, № 1 (2000): 141–51. http://dx.doi.org/10.1016/s1097-2765(00)80410-4.

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Pozsgai, Eric, Danielle Griffin, Kristin Heller, Jerry Mendell та Louise Rodino-Klapac. "622. Systemic β-Sarcoglycan Gene Therapy for Treatment of Cardiac and Skeletal Muscle Deficits in LGMD2E". Molecular Therapy 24 (травень 2016): S246—S247. http://dx.doi.org/10.1016/s1525-0016(16)33430-x.

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Pozsgai, Eric R., Danielle A. Griffin, Kristin N. Heller, Jerry R. Mendell та Louise R. Rodino-Klapac. "506. β-Sarcoglycan Gene Transfer Prevents Muscle Fibrosis and Inflammation in an Aged LGMD2E Mouse Model". Molecular Therapy 23 (травень 2015): S202—S203. http://dx.doi.org/10.1016/s1525-0016(16)34115-6.

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Fukai, Yuta, Yutaka Ohsawa, Hideaki Ohtsubo та ін. "Cleavage of β-dystroglycan occurs in sarcoglycan-deficient skeletal muscle without MMP-2 and MMP-9". Biochemical and Biophysical Research Communications 492, № 2 (2017): 199–205. http://dx.doi.org/10.1016/j.bbrc.2017.08.048.

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Gawlik, Kinga I., Johan Holmberg та Madeleine Durbeej. "Loss of Dystrophin and β-Sarcoglycan Significantly Exacerbates the Phenotype of Laminin α2 Chain–Deficient Animals". American Journal of Pathology 184, № 3 (2014): 740–52. http://dx.doi.org/10.1016/j.ajpath.2013.11.017.

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Wakayama, Y., Masahiko Inoue, Hiroko Kojima та ін. "Ultrastructural localization of α-, β- and γ-sarcoglycan and their mutual relation, and their relation to dystrophin, β-dystroglycan and β-spectrin in normal skeletal myofiber". Acta Neuropathologica 97, № 3 (1999): 288–96. http://dx.doi.org/10.1007/s004010050987.

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ter Laak, H. J., Q. H. Leyten, F. J. M. Gabreëls, H. Kuppen, W. O. Renier та R. C. A. Sengers. "Laminin-α2 (merosin), β-dystroglycan, α-sarcoglycan (adhalin), and dystrophin expression in congenital muscular dystrophies: An immunohistochemical study". Clinical Neurology and Neurosurgery 100, № 1 (1998): 5–10. http://dx.doi.org/10.1016/s0303-8467(97)00109-1.

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Hoshino, Sachiko, Norio Ohkoshi, Akiko Ishii та Shin'ichi Shoji. "The expression of dystrophin, α-sarcoglycan, and β-dystroglycan during skeletal muscle regeneration: immunohistochemical and western blot studies". Acta Histochemica 104, № 2 (2002): 139–47. http://dx.doi.org/10.1078/0065-1281-00620.

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Lovering, Richard M., and Patrick G. De Deyne. "Contractile function, sarcolemma integrity, and the loss of dystrophin after skeletal muscle eccentric contraction-induced injury." American Journal of Physiology-Cell Physiology 286, no. 2 (2004): C230—C238. http://dx.doi.org/10.1152/ajpcell.00199.2003.

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The purpose of this study was to evaluate the integrity of the muscle membrane and its associated cytoskeleton after a contraction-induced injury. A single eccentric contraction was performed in vivo on the tibialis anterior (TA) of male Sprague-Dawley rats at 900°/s throughout a 90°-arc of motion. Maximal tetanic tension (Po) of the TAs was assessed immediately and at 3, 7, and 21 days after the injury. To evaluate sarcolemmal integrity, we used an Evans blue dye (EBD) assay, and to assess structural changes, we used immunofluorescent labeling with antibodies against contractile (myosin, acti

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Sharma, Pawan, Thai Tran, Gerald L. Stelmack, et al. "Expression of the dystrophin-glycoprotein complex is a marker for human airway smooth muscle phenotype maturation." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 1 (2008): L57—L68. http://dx.doi.org/10.1152/ajplung.00378.2007.

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Airway smooth muscle (ASM) cells may contribute to asthma pathogenesis through their capacity to switch between a synthetic/proliferative and a contractile phenotype. The multimeric dystrophin-glycoprotein complex (DGC) spans the sarcolemma, linking the actin cytoskeleton and extracellular matrix. The DGC is expressed in smooth muscle tissue, but its functional role is not fully established. We tested whether contractile phenotype maturation of human ASM is associated with accumulation of DGC proteins. We compared subconfluent, serum-fed cultures and confluent cultures subjected to serum depri

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Ikeda, Yasuhiro, Maryann Martone, Yusu Gu, et al. "Altered membrane proteins and permeability correlate with cardiac dysfunction in cardiomyopathic hamsters." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 4 (2000): H1362—H1370. http://dx.doi.org/10.1152/ajpheart.2000.278.4.h1362.

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A mutation in the δ-sarcoglycan (SG) gene with absence of δ-SG protein in the heart has been identified in the BIO14.6 cardiomyopathic (CM) hamster, but how the defective gene leads to myocardial degeneration and dysfunction is unknown. We correlated left ventricular (LV) function with increased sarcolemmal membrane permeability and investigated the LV distribution of the dystrophin-dystroglycan complex in BIO14.6 CM hamsters. On echocardiography at 5 wk of age, the CM hamsters showed a mildly enlarged diastolic dimension (LVDD) with decreased LV percent fractional shortening (%FS), and at 9 w

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Assereto, Stefania, Silvia Stringara, Federica Sotgia, et al. "Pharmacological rescue of the dystrophin-glycoprotein complex in Duchenne and Becker skeletal muscle explants by proteasome inhibitor treatment." American Journal of Physiology-Cell Physiology 290, no. 2 (2006): C577—C582. http://dx.doi.org/10.1152/ajpcell.00434.2005.

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In this report, we have developed a novel method to identify compounds that rescue the dystrophin-glycoprotein complex (DGC) in patients with Duchenne or Becker muscular dystrophy. Briefly, freshly isolated skeletal muscle biopsies (termed skeletal muscle explants) from patients with Duchenne or Becker muscular dystrophy were maintained under defined cell culture conditions for a 24-h period in the absence or presence of a specific candidate compound. Using this approach, we have demonstrated that treatment with a well-characterized proteasome inhibitor, MG-132, is sufficient to rescue the exp

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Crippa, Stefania, Marco Cassano, Graziella Messina, et al. "miR669a and miR669q prevent skeletal muscle differentiation in postnatal cardiac progenitors." Journal of Cell Biology 193, no. 7 (2011): 1197–212. http://dx.doi.org/10.1083/jcb.201011099.

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Postnatal heart stem and progenitor cells are a potential therapeutic tool for cardiomyopathies, but little is known about the mechanisms that control cardiac differentiation. Recent work has highlighted an important role for microribonucleic acids (miRNAs) as regulators of cardiac and skeletal myogenesis. In this paper, we isolated cardiac progenitors from neonatal β-sarcoglycan (Sgcb)–null mouse hearts affected by dilated cardiomyopathy. Unexpectedly, Sgcb-null cardiac progenitors spontaneously differentiated into skeletal muscle fibers both in vitro and when transplanted into regenerating m

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O’Rourke, Erin, Louise Rodino-Klapac, Eric Pozsgai та ін. "eP212: Safety, β-Sarcoglycan expression, and functional outcomes from systemic gene transfer of rAAVrh74.MHCK7.hSGCB in LGMD2E/R4". Genetics in Medicine 24, № 3 (2022): S132—S133. http://dx.doi.org/10.1016/j.gim.2022.01.248.

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Pozsgai, Eric R., Danielle A. Griffin, Kristin N. Heller, Jerry R. Mendell та Louise R. Rodino-Klapac. "Systemic AAV-Mediated β-Sarcoglycan Delivery Targeting Cardiac and Skeletal Muscle Ameliorates Histological and Functional Deficits in LGMD2E Mice". Molecular Therapy 25, № 4 (2017): 855–69. http://dx.doi.org/10.1016/j.ymthe.2017.02.013.

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Sylvius, Nicolas, Laetitia Duboscq-Bidot, Christiane Bouchier та ін. "Mutational analysis of the β- and δ-sarcoglycan genes in a large number of patients with familial and sporadic dilated cardiomyopathy". American Journal of Medical Genetics Part A 120A, № 1 (2003): 8–12. http://dx.doi.org/10.1002/ajmg.a.20003.

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