| 品牌 | 货号 | 产品规格 | 价格(RMB) | 库存（上海） | 北京 | 武汉 | 南京 | 购买数量 |
|---|---|---|---|---|---|---|---|---|
| 源叶(MedMol) | S23408-1mg | 98% | ￥80.00元 | 10 | - | - | - |
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| 源叶(MedMol) | S23408-5mg | 98% | ￥110.00元 | 7 | - | - | - |
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| 源叶(MedMol) | S23408-10mg | 98% | ￥200.00元 | 7 | - | - | - |
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| 源叶(MedMol) | S23408-25mg | 98% | ￥400.00元 | 7 | - | - | - |
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| 源叶(MedMol) | S23408-100mg | 98% | ￥1060.00元 | 7 | - | - | - |
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| 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 | ||||||||||||||||||||
| 靶点： IGF-1R | ||||||||||||||||||||
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体外研究： 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. |
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体内研究： MID-1 does not have good pharmacokinetics in vivo. |
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参考文献： 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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| 溶解性： Soluble in DMSO | ||||||||||||||||||||
| 保存条件： -20℃ | ||||||||||||||||||||
配置溶液浓度参考：
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| 注意： | 部分产品我司仅能提供部分信息，我司不保证所提供信息的权威性，仅供客户参考交流研究之用。 |
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