Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function
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Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function. / Blazev, Ronnie; Carl, Christian Strini; Ng, Yaan-Kit; Molendijk, Jeffrey; Voldstedlund, Christian Thomas; Zhao, Yuanyuan; Xiao, Di; Kueh, Andrew J; Miotto, Paula M; Haynes, Vanessa R; Hardee, Justin P; Chung, Jin D; McNamara, James W; Qian, Hongwei; Gregorevic, Paul; Oakhill, Jonathan S; Herold, Marco J; Jensen, Thomas Elbenhardt; Lisowski, Leszek; Lynch, Gordon S; Dodd, Garron T; Watt, Matthew J; Yang, Pengyi; Kiens, Bente; Richter, Erik A.; Parker, Benjamin L.
I: Cell Metabolism, Bind 34, Nr. 10, 2022, s. 1561-1577.e9.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function
AU - Blazev, Ronnie
AU - Carl, Christian Strini
AU - Ng, Yaan-Kit
AU - Molendijk, Jeffrey
AU - Voldstedlund, Christian Thomas
AU - Zhao, Yuanyuan
AU - Xiao, Di
AU - Kueh, Andrew J
AU - Miotto, Paula M
AU - Haynes, Vanessa R
AU - Hardee, Justin P
AU - Chung, Jin D
AU - McNamara, James W
AU - Qian, Hongwei
AU - Gregorevic, Paul
AU - Oakhill, Jonathan S
AU - Herold, Marco J
AU - Jensen, Thomas Elbenhardt
AU - Lisowski, Leszek
AU - Lynch, Gordon S
AU - Dodd, Garron T
AU - Watt, Matthew J
AU - Yang, Pengyi
AU - Kiens, Bente
AU - Richter, Erik A.
AU - Parker, Benjamin L
N1 - Crown Copyright © 2022. Published by Elsevier Inc. All rights reserved.
PY - 2022
Y1 - 2022
N2 - Exercise induces signaling networks to improve muscle function and confer health benefits. To identify divergent and common signaling networks during and after different exercise modalities, we performed a phosphoproteomic analysis of human skeletal muscle from a cross-over intervention of endurance, sprint, and resistance exercise. This identified 5,486 phosphosites regulated during or after at least one type of exercise modality and only 420 core phosphosites common to all exercise. One of these core phosphosites was S67 on the uncharacterized protein C18ORF25, which we validated as an AMPK substrate. Mice lacking C18ORF25 have reduced skeletal muscle fiber size, exercise capacity, and muscle contractile function, and this was associated with reduced phosphorylation of contractile and Ca2+ handling proteins. Expression of C18ORF25 S66/67D phospho-mimetic reversed the decreased muscle force production. This work defines the divergent and canonical exercise phosphoproteome across different modalities and identifies C18ORF25 as a regulator of exercise signaling and muscle function.
AB - Exercise induces signaling networks to improve muscle function and confer health benefits. To identify divergent and common signaling networks during and after different exercise modalities, we performed a phosphoproteomic analysis of human skeletal muscle from a cross-over intervention of endurance, sprint, and resistance exercise. This identified 5,486 phosphosites regulated during or after at least one type of exercise modality and only 420 core phosphosites common to all exercise. One of these core phosphosites was S67 on the uncharacterized protein C18ORF25, which we validated as an AMPK substrate. Mice lacking C18ORF25 have reduced skeletal muscle fiber size, exercise capacity, and muscle contractile function, and this was associated with reduced phosphorylation of contractile and Ca2+ handling proteins. Expression of C18ORF25 S66/67D phospho-mimetic reversed the decreased muscle force production. This work defines the divergent and canonical exercise phosphoproteome across different modalities and identifies C18ORF25 as a regulator of exercise signaling and muscle function.
KW - Faculty of Science
KW - Exercise
KW - Skeletal muscle
KW - Phosphoproteomics
KW - AMPK
KW - C18ORF25
KW - Signaling
U2 - 10.1016/j.cmet.2022.07.003
DO - 10.1016/j.cmet.2022.07.003
M3 - Journal article
C2 - 35882232
VL - 34
SP - 1561-1577.e9
JO - Cell Metabolism
JF - Cell Metabolism
SN - 1550-4131
IS - 10
ER -
ID: 315181021