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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)
Publ. Version/Full Text Research data 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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Publication type Article: Journal article
Document type Scientific Article
Keywords 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
Journal Cell Reports
Quellenangaben Volume: 21, Issue: 6, Pages: 1507-1520 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge
Reviewing status Peer reviewed