Triadins are not triad-specific proteins: two new skeletal muscle triadins possibly involved in the architecture of sarcoplasmic reticulum.
Stéphane Vassilopoulos,Stéphane Vassilopoulos,Dominique Thevenon,Dominique Thevenon,Sophia Smida Rezgui,Sophia Smida Rezgui,Julie Brocard,Julie Brocard,Agnès Chapel,Alain Lacampagne,Joël Lunardi,Joël Lunardi,Michel DeWaard,Michel DeWaard,Isabelle Marty,Isabelle Marty +15 more
TL;DR: Two new triadin isoforms from rat skeletal muscle, Trisk 49 and Trisk 32, are cloned and could be involved in the set up and maintenance of a precise sarcoplasmic reticulum structure.
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About: This article is published in Journal of Biological Chemistry. The article was published on 05 Aug 2005. and is currently open access. The article focuses on the topics: Triadin & Longitudinal sarcoplasmic reticulum.
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Citations
Triadins Modulate Intracellular Ca2+ Homeostasis but Are Not Essential for Excitation-Contraction Coupling in Skeletal Muscle
Xiaohua Shen,Clara Franzini-Armstrong,Jose R. Lopez,Larry R. Jones,Yvonne M. Kobayashi,Yvonne M. Kobayashi,Ying Wang,W. Glenn L. Kerrick,Anthony H. Caswell,James D. Potter,Todd Miller,Paul D. Allen,Claudio F. Perez +12 more
TL;DR: The data support an indirect role for triadin in regulating myoplasmic Ca2+ homeostasis and organizing the molecular complex of the triad but not in regulating skeletal-type excitation-contraction coupling.
83
Sequential stages in the age-dependent gradual formation and accumulation of tubular aggregates in fast twitch muscle fibers: SERCA and calsequestrin involvement
TL;DR: The sequential stages leading to the initial appearance and maturation of TAs in EDL from male mice are investigated and it is suggested that the crystalline ATPase within the aggregates may be inactive.
71
Increased muscle stress-sensitivity induced by selenoprotein N inactivation in mouse: a mammalian model for SEPN1-related myopathy.
Mathieu Rederstorff,Perrine Castets,S. Arbogast,Jeanne Lainé,Stéphane Vassilopoulos,Maud Beuvin,Odile Dubourg,Alban Vignaud,Arnaud Ferry,Alain Krol,Valérie Allamand,Pascale Guicheney,Ana Ferreiro,Alain Lescure +13 more
TL;DR: This induced phenotype recapitulates the distribution of muscle involvement in patients with SEPN1-Related Myopathy, hence positioning this new animal model as a valuable tool to dissect the role of SelN in muscle function and to characterize the pathophysiological process.
Ca 2+ signaling in striated muscle: the elusive roles of triadin, junctin, and calsequestrin
TL;DR: The review of molecular interactions between calsequestrin, triadin, junctin and the ryanodine receptor in the lumen of the sarcoplasmic reticulum finds that cal sequestrin plays a different role in the heart and skeletal muscle, enhancing Ca2+ release in theHeart, but depressing Ca2- release in skeletal muscle.
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Junctin and triadin each activate skeletal ryanodine receptors but junctin alone mediates functional interactions with calsequestrin
TL;DR: It is shown that purified skeletal ryanodine receptors are similarly activated by purified triadin or purified junctin added to their luminal side, although a lack of competition indicated that the proteins act at independent sites.
59
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