Key result
Preventing Akt2-mediated Ankrd2 phosphorylation accelerates myogenic differentiation during oxidative stress.
Why the study?
Activation of Akt-mediated signaling pathways is crucial for muscle cell survival, differentiation, and regeneration, but novel specific substrates of Akt remain to be identified.
Population
C(2)C(12) murine muscle cells
Comparison
Phosphorylation-defective mutant Ankrd2 vs wild-type Ankrd2 under H2O2-induced oxidative stress
Design
Preclinical in vitro and in vivo molecular biology study
Authors
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Hypothesis-generating for redox control of myogenesis; leaves open therapeutic targeting in muscle disease.
Ankrd2 is identified as a novel Akt2-specific substrate that negatively regulates myogenesis in response to oxidative stress.
Cenni et al. (2011) studied Oxidative stress and myogenic differentiation. H2O2-induced oxidative stress and forced expression of phosphorylation-defective Ankrd2 mutant was evaluated on Ankrd2 phosphorylation and myogenic differentiation. Akt2 specifically phosphorylates Ankrd2 at Ser-99 in response to H2O2-induced oxidative stress, and a phosphorylation-defective Ankrd2 mutant promoted faster myogenic differentiation.
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