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Clarke, K.* ; Ricciardi, S.* ; Pearson, T.* ; Bharudin, I.* ; Davidsen, P.K.* ; Bonomo, M.* ; Brina, D.* ; Scagliola, A.* ; Simpson, D.M.* ; Beynon, R.J.* ; Khanim, F.* ; Ankers, J.* ; Sarzynski, M.A.* ; Ghosh, S.* ; Pisconti, A.* ; Rozman, J. ; Hrabě de Angelis, M. ; Bunce, C.* ; Stewart, C.* ; Egginton, S.* ; Caddick, M.* ; Jackson, M.A.* ; Bouchard, C.* ; Biffo, S.* ; Falciani, F.*

The role of Eif6 in skeletal muscle homeostasis revealed by endurance training co-expression networks.

Cell Rep. 21, 1507-1520 (2017)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
Regular endurance training improves muscle oxidative capacity and reduces the risk of age-related disorders. Understanding the molecular networks underlying this phenomenon is crucial. Here, by exploiting the power of computational modeling, we show that endurance training induces profound changes in gene regulatory networks linking signaling and selective control of translation to energy metabolism and tissue remodeling. We discovered that knockdown of the mTOR-independent factor Eif6, which we predicted to be a key regulator of this process, affects mitochondrial respiration efficiency, ROS production, and exercise performance. Our work demonstrates the validity of a data-driven approach to understanding muscle homeostasis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Eif6 ; Exercise ; Metabolism ; Mitochondria ; Network Biology ; Skeletal Muscle ; Systems Biology; Fiber-type; Insulin Sensitivity; Messenger-rna; Translation; Metabolism; Exercise; Gene; Capacity; Resistance; Expression
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 21, Heft: 6, Seiten: 1507-1520 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge
Begutachtungsstatus Peer reviewed