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MID-1
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
MID-1图片
CAS NO:312608-54-1
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议

产品介绍
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。
Cas No.312608-54-1
Canonical SMILESO=C(NC1=NC=C([N+]([O-])=O)S1)C2=CC=C(OCC)C=C2
分子式C12H11N3O4S
分子量293.3
溶解度DMSO: 31.25 mg/mL (106.55 mM)
储存条件Store at -20℃
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

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.