IRES-C11 是一种特异的 c-MYC 内部核糖体进入位点 (IRES) 翻译抑制剂。IRES-C11 阻断必需的 c-MYC IRES 反式作用因子、异质核核糖核蛋白 A1 与其 IRES 的相互作用。IRES-C11 不抑制 BAG-1、XIAP 和 p53 IRESes。

IRES-C11 is a spectfic c-MYC internal ribosome entry site (IRES) translation inhibitor. IRES-C11 blocks the interaction of a requisite c-MYC IRES trans-acting factor, heterogeneous nuclear ribonucleoprotein A1, with its IRES. IRES-C11 does not inhibits BAG-1, XIAP and p53 IRESes.

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IRES-C11 blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic anti-glioblastoma properties when combined with the mechanistic target of mTOR PP242.
IRES-C11 (50 nM) significantly inhibits both cyclin D1 and c-MYC IRES activity. IRES-C11 treatment induces a significant shift in both cyclin D1 and c-MYC mRNA to monosomal/nonribosomal fractions, whereas actin mRNA distribution is unaffected. IRES-C11 inhibits both cyclin D1 and c-MYC IRES-mediated mRNA translation, leading to reductions in protein levels.
Mechanistic studies with IRES-C11 reveal binding of the inhibitors within the UP1 fragment of heterogeneous nuclear ribonucleoprotein A1. has not independently confirmed the accuracy of these methods. They are for reference only.

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Powder -20°C 3 years；In solvent -80°C 6 months

[1]. Brent Holmes, et al. Mechanistic Target of Rapamycin (mTOR) Inhibition Synergizes with Reduced Internal Ribosome Entry Site (IRES)-mediated Translation of Cyclin D1 and c-MYC mRNAs to Treat Glioblastoma. J Biol Chem. 2016 Jul 1;291(27):14146-14159.
[2]. Y Shi, et al. Therapeutic potential of targeting IRES-dependent c-myc translation in multiple myeloma cells during ER stress. Oncogene. 2016 Feb 25;35(8):1015-24.

In Vitro: DMSO : 250 mg/mL (790.79 mM; Need ultrasonic)配制储备液