首页> 外国专利> E2EPF ubiquitin carrier protein-von Hippel-Lindau interaction and uses of thereof

E2EPF ubiquitin carrier protein-von Hippel-Lindau interaction and uses of thereof

机译:E2EPF泛素载体蛋白-von Hippel-Lindau相互作用及其应用

摘要

The present invention relates to the E2EPF UCP-VHL interaction and the uses thereof, more precisely a method for increasing or reducing VHL activity or level by regulating UCP activity or level to inhibit cancer cell proliferation or metastasis or to increase angiogenesis. The inhibition of UCP activity is accomplished by any UCP activity inhibitor selected from a group consisting of a small interfering RNA (RNAi), an antisense oligonucleotide, and a polynucleotide complementarily binding to mRNA of UCP, a peptide, a peptide mimetics and an antibody, and a low molecular compound. In the meantime, the increase of angiogenesis is accomplished by the following mechanism; UCP over-expression is induced by a gene carrier and thus endogenous VHL is reduced, leading to the stabilization of HIF-la which enhances VEGF activation based on the HIF-1± stabilization. The method for regulating UCP activity or level results in the increase or decrease of VHL activity or level, so that it can be applied to the development of an anticancer agent and an angiogenesis inducer.
机译:本发明涉及E2EPF UCP-VHL相互作用及其用途,更准确地说,涉及通过调节UCP活性或水平以抑制癌细胞增殖或转移或增加血管生成来增加或降低VHL活性或水平的方法。可以通过选自小干扰RNA(RNAi),反义寡核苷酸和与UCP mRNA,肽,肽模拟物和抗体互补结合的多核苷酸的任何UCP活性抑制剂来实现对UCP活性的抑制。和低分子化合物。同时,血管生成的增加是通过以下机制完成的:基因载体诱导UCP过表达,从而降低内源性VHL,从而导致HIF-1α的稳定化,从而基于HIF-1±稳定化增强了VEGF的激活。调节UCP活性或水平的方法导致VHL活性或水平的增加或降低,因此其可用于开发抗癌剂和血管生成诱导剂。

著录项

  • 公开/公告号KR100877824B1

    专利类型

  • 公开/公告日2009-01-12

    原文格式PDF

  • 申请/专利权人

    申请/专利号KR20050108014

  • 发明设计人 임동수;정초록;황경선;

    申请日2005-11-11

  • 分类号C07K1;C07K1/06;C12N15/86;C12N15/867;

  • 国家 KR

  • 入库时间 2022-08-21 19:12:15

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