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2. 发明申请

WO2007055547A1 E2EPF UBIQUITIN CARRIER PROTEIN-VON HIPPEL-LINDAU INTERACTION AND USES OF THEREOF 审中-公开
标题翻译： E2EPF UBIQUITIN载体蛋白质 - 肛门 - 林达相互作用及其用途
公开(公告)号：WO2007055547A1
公开(公告)日：2007-05-18
申请号：PCT/KR2006/004749
申请日：2006-11-13
申请人： KOREA RESEARCH INSTITUTE OF BIOSCIENCE AND BIOTECHNOLOGY , IM, Dong-Soo , JUNG, Cho-Rok , HWANG, Kyung-Sun
发明人： IM, Dong-Soo , JUNG, Cho-Rok , HWANG, Kyung-Sun
IPC分类号： C07K1/00
CPC分类号： C12N9/93 , C07K14/4703 , C07K14/4738 , C12N15/1137 , C12N2310/111 , C12N2310/14 , C12Y603/02019
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- lα which enhances VEGF activation based on the HIF- lα 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.
摘要翻译：本发明涉及E2EPF UCP-VHL相互作用及其用途，更确切地说，涉及通过调节UCP活性或抑制癌细胞增殖或转移或增加血管生成的水平来增加或降低VHL活性或水平的方法。 UCP活性的抑制是通过选自小干扰RNA（RNAi），反义寡核苷酸和与UCP mRNA，肽，模拟物和抗体互补结合的多核苷酸的任何UCP活性抑制剂完成的，和低分子化合物。同时，通过以下机制实现血管生成的增加; UCP过表达由基因载体诱导，因此内源性VHL被还原，导致HIF-1a的稳定化，其增强了基于HIF-1α稳定化的VEGF活化。调节UCP活性或水平的方法导致VHL活性或水平的增加或减少，从而可以应用于抗癌剂和血管发生诱导剂的开发。

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