%0 Journal Article %T Retrograde regulation of store-operated calcium channels by the ryanodine receptor-associated protein triadin 95 in rat skeletal myotubes. %+ Canaux calciques , fonctions et pathologies %+ Généthon %+ Laboratoire de biophysique moléculaire et cellulaire (LBMC) %A Vassilopoulos, Stéphane %A Brocard, Julie %A Garcia, Luis %A Marty, Isabelle %A Bouron, Alexandre %Z Thisworkwas partly supported by grants from the Association Franc¸aise contre les Myopathies (AFM), la Fondation pour la Recherche M'edicale as well as by grants from the GIS-Institut des Maladies Rares. %< avec comité de lecture %@ 0143-4160 %J Cell Calcium %I Elsevier %V 41 %N 2 %P 179-85 %8 2007-02 %D 2007 %R 10.1016/j.ceca.2006.06.003 %M 16889828 %K Triadin %K Store-operated channels %K Calcium %Z Life Sciences [q-bio]/Biochemistry, Molecular BiologyJournal articles %X The 95kDa triadin (or T95), the main skeletal muscle triadin isoform, negatively regulates the mechanism of excitation-contraction coupling. T95 is a ryanodine receptor (RyR)-interacting protein but it also possesses a calsequestrin-interacting domain. RyR and calsequestrin are involved in Ca2+ signalling and, for instance, influence the activity of store-dependent Ca2+ channels (SOC). This work was undertaken to determine whether T95 was able to modulate the entry of Ca2+ through SOC. The experiments were carried out on differentiated rat myotubes over-expressing T95 or DsRed (control cells) by means of an adenovirus infection. Intracellular Ca2+ signals were analyzed using the Ca2+ indicator Fluo-4. The sarco-endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin was used to deplete intracellular Ca2+ stores. When applied in the presence of a Ca2+-free medium, thapsigargin elicited transient but long-lasting Fluo-4 responses by elevating the cytoplasmic concentration of Ca2+ ([Ca2+]i). The over-expression of T95 reduced the thapsigargin-dependent [Ca2+]i increase, with respect to control myotubes. Addition of extracellular Ca2+after the depletion of this Ca2+ pool was accompanied by a [Ca2+]i increase that was sensitive to the SOC blockers 2-APB, SKF-96365 and La3+. The over-expression of T95 reduced this Ca2+ influx, without changing its pharmacological properties, showing that T95 over-expression did not alter the properties of the SOC. In conclusion, the RyR-interacting molecule T95, recently shown to inhibit the excitation-contraction coupling, has also the ability to interfere with the skeletal muscle Ca2+ signalling by depressing thapsigargin-dependent Ca2+ release and influx. %G English %2 https://inserm.hal.science/inserm-00380044/document %2 https://inserm.hal.science/inserm-00380044/file/Vassilopoulos_2007.pdf %L inserm-00380044 %U https://inserm.hal.science/inserm-00380044 %~ INSERM %~ CEA %~ UGA %~ CNRS %~ UNIV-GRENOBLE1 %~ U836 %~ FRM