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The phosphorylated SMAD2/3 (pSMAD2/3) then forms a complex with SMAD4,[66] which translocates to the nucleus to regulate gene expression, thereby negatively regulating myoblast proliferation,[14] differentiation, and fusion.[67] MSTN signaling can be inhibited by (1) blocking the interaction between the active C-terminal dimer and ActRIIA/B, as seen with anti-MSTN antibodies such as MYO-029 and landogrozumab
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