Title : Phosphorylation of ERK and dystrophin S3059 protects against inflammation-associated C2C12 myotube atrophy.

Pub. Date : 2021 Jun 1

PMID : 33729835






4 Functional Relationships(s)
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1 Increased ERK activation by addition of phorbol myristate acetate (PMA) also reduced inflammation-associated myotube atrophy, and increased the interaction between dystrophin and beta-dystroglycan, which was partially attenuated in the presence of a phosphomimetic mutation at dystrophin S3059. Tetradecanoylphorbol Acetate dystrophin, muscular dystrophy Mus musculus
2 Increased ERK activation by addition of phorbol myristate acetate (PMA) also reduced inflammation-associated myotube atrophy, and increased the interaction between dystrophin and beta-dystroglycan, which was partially attenuated in the presence of a phosphomimetic mutation at dystrophin S3059. Tetradecanoylphorbol Acetate dystrophin, muscular dystrophy Mus musculus
3 Increased ERK activation by addition of phorbol myristate acetate (PMA) also reduced inflammation-associated myotube atrophy, and increased the interaction between dystrophin and beta-dystroglycan, which was partially attenuated in the presence of a phosphomimetic mutation at dystrophin S3059. Tetradecanoylphorbol Acetate dystrophin, muscular dystrophy Mus musculus
4 Increased ERK activation by addition of phorbol myristate acetate (PMA) also reduced inflammation-associated myotube atrophy, and increased the interaction between dystrophin and beta-dystroglycan, which was partially attenuated in the presence of a phosphomimetic mutation at dystrophin S3059. Tetradecanoylphorbol Acetate dystrophin, muscular dystrophy Mus musculus