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Littérature scientifique sur le sujet « Β-sarcoglycan »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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Articles de revues sur le sujet "Β-sarcoglycan"

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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Thèses sur le sujet "Β-sarcoglycan"

GIBERTINI, SARA. "Characterization and comparison of muscle fibrosis in two mouse models and In Vivo test of an anti-fibrotic molecule." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/94571.

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Muscle fibrosis, a hallmark of severe muscular dystrophies, is a mechanism not completely understood, characterized by marked deposition of collagens and other extracellular matrix (ECM) components, progressively replacing muscle fibres. Fibrosis also occurs in other human conditions affecting different organs/tissues including liver, heart, kidney and lung. In skeletal and cardiac muscle, dystrophin is associated with a large complex of sarcolemmal and cytoskeletal proteins, the dystrophin-glycoprotein complex (DGC), that confers a structural link between the laminin-α2 in the ECM and the c

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Actes de conférences sur le sujet "Β-sarcoglycan"

Rodino-Klapac, L. R., E. R. Pozsgai, S. Lewis та ін. "Safety, β-Sarcoglycan Expression, and Functional Outcomes from Systemic Gene Transfer of rAAVrh74.MHCK7.hSGCB in LGMD2E/R4". У Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739648.

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