| 规格: | 98% |
| 分子量: | 316.14 |
| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
Background:
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[1][2].
IRES-C11 blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic anti-glioblastoma properties when combined with the mechanistic target of mTOR PP242[1].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.
[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.
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