MID-1 是一种 MG53-IRS-1 (Mitsugumin 53-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。

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.

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MID-1 (5 μM; 24 h) increases the IRS-1 expression level in skeletal muscle by disrupting the MG53-IRS-1 interaction.
MID-1 (10 μM; 12 h) reduces the luciferase activity in HEK 293 cell line expressing NLUC-IRS-1 and CLUC-C14A.
MID-1 (1-20 μM; 12 h) disrupts the MG53-IRS-1 interaction but not MG53-FAK interaction in HEK 293 cells.
MID-1 (0.1-10 μM; 4-24 h) abolishes MG53-induced IRS-1 ubiquitination and degradation in HEK 293 cells.
MID-1 (5-10 μM; 24 h) increases insulin signaling and insulin-elicited glucose uptake in C2C12 myotubes.
MID-1 (5-10 μM; 24 h) enhances skeletal myogenesis. has not independently confirmed the accuracy of these methods. They are for reference only.

MID-1 does not have good pharmacokinetics in vivo. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[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.

In Vitro: DMSO : 31.25 mg/mL (106.55 mM; Need ultrasonic)配制储备液