Régulations post-transcriptionnelles et nutrition

@inbook{,

title = {What do we know about selenium contribution to muscle physiology?},

author = {A Lescure and M Briens and A Ferreiro},

editor = {D L Hatfield and U Schweizer and P A Tsuji and V Gladyshev},

url = {http://link.springer.com/chapter/10.1007/978-3-319-41283-2_40},

doi = {10.1007/978-3-319-41283-2_40},

year  = {2016},

date = {2016-01-01},

booktitle = {Selenium: Its molecular biology and role in human health},

pages = {475-486},

publisher = {Springer},

edition = {4},

abstract = {Early observations of selenium (Se) deficiencies in human and livestock revealed the importance of this trace element for normal muscle function. However, the molecular and cellular dysfunction connecting low selenium diets to muscular diseases remain elusive. Importantly, mutations in the SEPN1 gene encoding selenoprotein N (SEPN1) were shown to cause an inherited muscular disease in humans. Therefore, it is expected that understanding the role of SEPN1 and the related pathophysiology will unveil the participation of Se in molecular processes essential for muscle function and pave the way for targeted therapeutics. However, the functional characterization of SEPN1 is still lacking. Analysis of its activity in cellular and animal models pointed to its involvement in oxidative stress defense and in control of calcium (Ca2+) handling. A link between the activities of SEPN1 and of the Ca2+ transporters, RyR1 and SERCA, was shown, but the enzymatic reaction catalyzed by SEPN1 has not been characterized.},

keywords = {Intracellular calcium handling Muscle Muscular dystrophies Oxidative stress Selenium Selenoprotein N, LESCURE, Unité ARN},

pubstate = {published},

tppubtype = {inbook}

}