ArticleThe Biochemical journal2004
Characterization of the ATP-hydrolysing activity of alpha-sarcoglycan.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Repairing the defective folding of alpha-sarcoglycan is needed to promote myogenic cell engraftment in 3D artificial muscle models of LGMDR3.Skeletal muscle · 2025Article
- Genetic Deletion of the Purinergic ReceptorACS pharmacology & translational science · 2025Article
- Sarcospan protects against LGMD R5 via remodeling of the sarcoglycan complex composition in dystrophic mice.The Journal of clinical investigation · 2025Article
- Sarcoglycans are enriched at the neuromuscular junction in a nerve-dependent manner.Cell death & disease · 2025Article
- Thrombospondin-4 deletion does not exacerbate muscular dystrophy in β-sarcoglycan-deficient and laminin α2 chain-deficient mice.Scientific reports · 2024Article
- The Role of P2X7 Purinoceptors in the Pathogenesis and Treatment of Muscular Dystrophies.International journal of molecular sciences · 2023Review
- P2 Receptor Signaling in Motor Units in Muscular Dystrophy.International journal of molecular sciences · 2023Review
- Mechanisms of Myofibre Death in Muscular Dystrophies: The Emergence of the Regulated Forms of Necrosis in Myology.International journal of molecular sciences · 2022Review
- CFTR corrector C17 is effective in muscular dystrophy, in vivo proof of concept in LGMDR3.Human molecular genetics · 2022Article
- P2X7 Receptor Antagonist Reduces Fibrosis and Inflammation in a Mouse Model of Alpha-Sarcoglycan Muscular Dystrophy.Pharmaceuticals (Basel, Switzerland) · 2022Article
- eATP/P2X7R Axis: An Orchestrated Pathway Triggering Inflammasome Activation in Muscle Diseases.International journal of molecular sciences · 2020Review
- Combined Use of CFTR Correctors in LGMD2D Myotubes Improves Sarcoglycan Complex Recovery.International journal of molecular sciences · 2020Article
- The Danger Signal Extracellular ATP Is Involved in the Immunomediated Damage of α-Sarcoglycan-Deficient Muscular Dystrophy.The American journal of pathology · 2019Article
- Repairing folding-defective α-sarcoglycan mutants by CFTR correctors, a potential therapy for limb-girdle muscular dystrophy 2D.Human molecular genetics · 2018Article
- Dystrophin: The dead calm of a dogma.Rare diseases (Austin, Tex.) · 2016Article
- P2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophy.PLoS medicine · 2015Article
- The Dystrophin Complex: Structure, Function, and Implications for Therapy.Comprehensive Physiology · 2015Review
- Pannexin channels mediate the acquisition of myogenic commitment in C2C12 reserve cells promoted by P2 receptor activation.Frontiers in cell and developmental biology · 2015Article
- A novel mechanism of autophagic cell death in dystrophic muscle regulated by P2RX7 receptor large-pore formation and HSP90.Autophagy · 2015Article
- Finding the sweet spot: assembly and glycosylation of the dystrophin-associated glycoprotein complex.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha-Sarcoglycan is a glycoprotein associated with the dystrophin complex at sarcolemma of skeletal and cardiac muscles. Gene defects in alpha-sarcoglycan lead to a severe muscular dystrophy whose molecular mechanisms are not yet clear. A first insight into the function of alpha-sarcoglycan was obtained by finding that it is an ATP-binding protein and that it probably confers ability to hydrolyse ATP to the purified dystrophin complex [Betto, Senter, Ceoldo, Tarricone, Biral and Salviati (1999) J. Biol. Chem. 274, 7907-7912]. In the present study, we present definitive evidence showing that alpha-sarcoglycan is an ATP-hydrolysing enzyme. The appearance of alpha-sarcoglycan protein expression was correlated with the increase in ecto-nucleotidase activity during differentiation of C2C12 cells. Approx. 25% of ecto-nucleotidase activity displayed by the C2C12 myotubes was inhibited by preincubating cells with an antibody specific for the ATP-binding motif of alpha-sarcoglycan. This demonstrates that alpha-sarcoglycan substantially contributes to total ecto-nucleotidase activity of C2C12 myotubes. To characterize further this activity, human embryonic kidney 293 cells were transfected with expression plasmids containing alpha-sarcoglycan cDNA. Transfected cells exhibited a significant increase in the ATP-hydrolysing activity that was abolished by the anti-alpha-sarcoglycan antibody. The enzyme had a substrate specificity for ATP and ADP, did not hydrolyse other triphosphonucleosides, and the affinity for ATP was in the low mM range. The ATPase activity strictly required the presence of both Mg2+ and Ca2+ and was completely inhibited by suramin and reactive blue-2. These results show that alpha-sarcoglycan is a Ca2+, Mg2+-ecto-ATPDase. The possible consequences of the absence of alpha-sarcoglycan activity in the pathogenesis of muscular dystrophy are discussed.
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