PI 3-kinase acts as an upstream mediator that is both necessary and rate-limiting for the process of myogenesis and the expression of muscle-specific genes.
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No immediate clinical implications for muscle disorders; leaves open PI 3-kinase as a myogenesis regulator for human studies.
The oncogene p3k, coding for a constitutively active form of phosphatidylinositol 3-kinase (PI 3-kinase; EC 2.7.1.137), strongly enhances myogenic differentiation in cultures of chicken-embryo myoblasts. It increases the size of the myotubes and induces elevated levels of the muscle-specific proteins MyoD, myosin heavy chain, creatine kinase, and desmin. Inhibition of PI 3-kinase activity with LY294002 or with dominant-negative mutants of PI 3-kinase interferes with myogenic differentiation and with the induction of muscle-specific genes. PI 3-kinase is therefore an upstream mediator for the expression of the muscle-specific genes and is both necessary and rate-limiting for the process of myogenesis.
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Jiang et al. (1998) studied this question.
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