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Triadin: what possible function 20 years later?
Author(s) -
Marty Isabelle,
Fauré Julien,
FourestLieuvin Anne,
Vassilopoulos Stéphane,
Oddoux Sarah,
Brocard Julie
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.171892
Subject(s) - ryanodine receptor , skeletal muscle , neuroscience , biology , anatomy , endoplasmic reticulum , microbiology and biotechnology
During the last 20 years, the identification of triadin function in cardiac and skeletal muscle has been the focus of numerous studies. First thought of as the missing link between the ryanodine receptor and the dihydropyridine receptor and responsible of skeletal type excitation–contraction coupling, the current hypothesis on triadin function has slowly evolved, and triadin is envisaged now as a regulator of calcium release, both in cardiac and skeletal muscle. Nevertheless, none of the experiments performed up to now has given a clear cut view of what triadin really does in muscle. The problem became more complex with the identification of multiple triadin isoforms, having possibly multiple functions. Using a different approach from what has been done previously, we have obtained new clues about the function of triadin. Our data point to a possible involvement of triadin in reticulum structure, in relation with the microtubule network.