These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Retrograde regulation of store-operated calcium channels by the ryanodine receptor-associated protein triadin 95 in rat skeletal myotubes. Author: Vassilopoulos S, Brocard J, Garcia L, Marty I, Bouron A. Journal: Cell Calcium; 2007 Feb; 41(2):179-85. PubMed ID: 16889828. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]