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MID-1 is a disruptor of MG53-IRS-1 (Mitsugumin 53-insulin receptor substrate-1) interaction. MID-1 disrupts molecular association of MG53 with IRS-1 and abolishes MG53-induced IRS-1 ubiquitination and degradation in skeletal muscle, leading to elevated IRS-1 expression level and increased insulin signaling and glucose uptake[1].

MID-1 (5 μM; 24 h) increases the IRS-1 expression level in skeletal muscle by disrupting the MG53-IRS-1 interaction[1].MID-1 (10 μM; 12 h) reduces the luciferase activity in HEK 293 cell line expressing NLUC-IRS-1 and CLUC-C14A[1].MID-1 (1-20 μM; 12 h) disrupts the MG53-IRS-1 interaction but not MG53-FAK interaction in HEK 293 cells[1].MID-1 (0.1-10 μM; 4-24 h) abolishes MG53-induced IRS-1 ubiquitination and degradation in HEK 293 cells[1].MID-1 (5-10 μM; 24 h) increases insulin signaling and insulin-elicited glucose uptake in C2C12 myotubes[1].MID-1 (5-10 μM; 24 h) enhances skeletal myogenesis[1]. Western Blot Analysis[1] Cell Line: C2C12 myotubes

MID-1 does not have good pharmacokinetics in vivo[1].

[1]. Lee H, et, al. MG53-IRS-1 (Mitsugumin 53-Insulin Receptor Substrate-1) Interaction Disruptor Sensitizes Insulin Signaling in Skeletal Muscle. J Biol Chem. 2016 Dec 23;291(52):26627-26635.

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