MID-1是一种MG53-IRS-1(Mitsugumin53-胰岛素受体底物1)相互作用的抑制剂。MID-1破坏了MG53与IRS-1的分子缔合，并消除了MG53诱导的IRS-1泛素化和骨骼肌降解，从而导致IRS-1表达水平升高，胰岛素信号传导和葡萄糖摄取增加。
货号:ajcx31922
CAS:312608-54-1
分子式:C12H11N3O4S
分子量：293.3
溶解度:DMSO: 31.25 mg/mL (106.55 mM)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

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.