Proteomics

Dataset Information

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Triggering acute RyR1 Ca2+ leak leads to improved mitochondrial remodelling and function


ABSTRACT: C2C12 myotubes at day 7 of differentiation were stimulated with a single session of SIT (6 x 30s with 4 min at rest) and were immediately after the stimulation treated or not with 10 uM S107 drug for 72h. The myotubes were then harvested at 72h post stimulation (for SIT condition) and 72h post stimulation and S107 treatment (for SIT S107 condition) for mass spectrometry analysis using the proteomics approach. N = 5 independent myotube wells per condition.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skeletal Muscle Cell

SUBMITTER: Manfredo Quadroni  

LAB HEAD: Nicolas Place

PROVIDER: PXD018409 | Pride | 2021-10-20

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
191211_Zanou_11877_01.raw Raw
191211_Zanou_11877_02.raw Raw
191211_Zanou_11877_03.raw Raw
191211_Zanou_11877_04.raw Raw
191211_Zanou_11877_05.raw Raw
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Publications


Sustained ryanodine receptor (RyR) Ca<sup>2+</sup> leak is associated with pathological conditions such as heart failure or skeletal muscle weakness. We report that a single session of sprint interval training (SIT), but not of moderate intensity continuous training (MICT), triggers RyR1 protein oxidation and nitrosylation leading to calstabin1 dissociation in healthy human muscle and in in vitro SIT models (simulated SIT or S-SIT). This is accompanied by decreased sarcoplasmic reticulum Ca<sup>  ...[more]

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