公开(公告)号：US09066976B2

公开(公告)日：2015-06-30

申请号：US13215085

申请日：2011-08-22

申请人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang ,  Jung Hwa Lim

发明人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang ,  Jung Hwa Lim

IPC分类号： A61K48/00 ,  C07K14/00 ,  C07H21/04 ,  A61K38/53 ,  C07K14/47 ,  C12N9/00 ,  C12N15/85

CPC分类号： A61K48/005 ,  A61K38/53 ,  C07K14/4703 ,  C07K14/4738 ,  C12N9/93 ,  C12N15/1137 ,  C12N15/85 ,  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-1α which enhances VEGF activation based on the HIF-1α 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.

公开(公告)号：US08088750B2

公开(公告)日：2012-01-03

申请号：US12704226

申请日：2010-02-11

申请人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

发明人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

IPC分类号： C12N15/11

CPC分类号： A61K31/00 ,  A61K31/7088 ,  C12N15/113 ,  C12N2310/14 ,  C12Q1/6886 ,  C12Q2600/136 ,  C12Q2600/158 ,  G01N33/5011 ,  G01N33/574 ,  G01N2500/02

摘要： The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by to selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

摘要翻译： 本发明涉及谜（PDLIM7）-Mdm2的相互作用及其用途。 更具体地，其可以通过抑制诱导Mdm2不稳定和p53活性的Enigma表达或Enigma活性来诱导癌细胞的有效凋亡; 它可以通过确定SRF诱导的Enigma在具有Mdm2的癌组织中过表达来评估抗癌治疗的预后; 它可以通过选择抑制Enigma和Mdm2之间特异性结合的因子来筛选抗癌活性物质。 Enigma-Mdm2相互作用和Enigma表达调控可有效地用于预防癌症和开发治疗方法和抗癌剂。

公开(公告)号：US20100239566A1

公开(公告)日：2010-09-23

申请号：US12704226

申请日：2010-02-11

申请人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

发明人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

IPC分类号： A61K39/395 ,  A61K31/7088 ,  A61P35/04 ,  A61K38/00 ,  G01N33/53

CPC分类号： A61K31/00 ,  A61K31/7088 ,  C12N15/113 ,  C12N2310/14 ,  C12Q1/6886 ,  C12Q2600/136 ,  C12Q2600/158 ,  G01N33/5011 ,  G01N33/574 ,  G01N2500/02

摘要： The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by to selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

摘要翻译： 本发明涉及谜（PDLIM7）-Mdm2相互作用及其用途。 更具体地，其可以通过抑制诱导Mdm2不稳定和p53活性的Enigma表达或Enigma活性来诱导癌细胞的有效凋亡; 它可以通过确定SRF诱导的Enigma在具有Mdm2的癌组织中过表达来评估抗癌治疗的预后; 它可以通过选择抑制Enigma和Mdm2之间特异性结合的因子来筛选抗癌活性物质。 Enigma-Mdm2相互作用和Enigma表达调控可有效地用于预防癌症和开发治疗方法和抗癌剂。

公开(公告)号：US08404435B2

公开(公告)日：2013-03-26

申请号：US13240351

申请日：2011-09-22

申请人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

发明人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

IPC分类号： C12Q1/68 ,  G01N33/53

CPC分类号： A61K31/00 ,  A61K31/7088 ,  C12N15/113 ,  C12N2310/14 ,  C12Q1/6886 ,  C12Q2600/136 ,  C12Q2600/158 ,  G01N33/5011 ,  G01N33/574 ,  G01N2500/02

摘要： The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

摘要翻译： 本发明涉及谜（PDLIM7）-Mdm2相互作用及其用途。 更具体地，其可以通过抑制诱导Mdm2不稳定和p53活性的Enigma表达或Enigma活性来诱导癌细胞的有效凋亡; 它可以通过确定SRF诱导的Enigma在具有Mdm2的癌组织中过表达来评估抗癌治疗的预后; 它可以通过选择抑制Enigma和Mdm2之间特异性结合的因子来筛选抗癌活性物质。 Enigma-Mdm2相互作用和Enigma表达调控可有效地用于预防癌症和开发治疗方法和抗癌剂。

公开(公告)号：US20120015374A1

公开(公告)日：2012-01-19

申请号：US13240351

申请日：2011-09-22

申请人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

发明人： Cho-Rok Jung ,  Dong-Soo Im ,  Jung-Hwa Lim ,  Yoon Jung Choi

IPC分类号： G01N33/566 ,  C12Q1/02

CPC分类号： A61K31/00 ,  A61K31/7088 ,  C12N15/113 ,  C12N2310/14 ,  C12Q1/6886 ,  C12Q2600/136 ,  C12Q2600/158 ,  G01N33/5011 ,  G01N33/574 ,  G01N2500/02

摘要： The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

摘要翻译： 本发明涉及谜（PDLIM7）-Mdm2相互作用及其用途。 更具体地，其可以通过抑制诱导Mdm2不稳定和p53活性的Enigma表达或Enigma活性来诱导癌细胞的有效凋亡; 它可以通过确定SRF诱导的Enigma在具有Mdm2的癌组织中过表达来评估抗癌治疗的预后; 它可以通过选择抑制Enigma和Mdm2之间特异性结合的因子来筛选抗癌活性物质。 Enigma-Mdm2相互作用和Enigma表达调控可有效地用于预防癌症和开发治疗方法和抗癌剂。

公开(公告)号：US20110213016A1

公开(公告)日：2011-09-01

申请号：US12789670

申请日：2010-05-28

申请人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

发明人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

IPC分类号： A61K48/00

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-1α which enhances VEGF activation based on the HIF-1α 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，导致基于HIF-1α稳定增强VEGF活化的HIF-1α的稳定性。 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。

公开(公告)号：US20080269158A1

公开(公告)日：2008-10-30

申请号：US12093093

申请日：2006-11-13

申请人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

发明人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

IPC分类号： A61K31/7105 ,  C12Q1/68 ,  C12Q1/02 ,  C12P21/06

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-1α which enhances VEGF activation based on the HIF-1α 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-1α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。

公开(公告)号：US20120107297A1

公开(公告)日：2012-05-03

申请号：US13215085

申请日：2011-08-22

申请人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

发明人： Dong-Soo Im ,  Cho-Rok Jung ,  Kyung-Sun Hwang

IPC分类号： A61K38/53 ,  A61P9/10 ,  A61K48/00 ,  A61P9/00

CPC分类号： A61K48/005 ,  A61K38/53 ,  C07K14/4703 ,  C07K14/4738 ,  C12N9/93 ,  C12N15/1137 ,  C12N15/85 ,  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-1α which enhances VEGF activation based on the HIF-1α 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，导致基于HIF-1α稳定增强VEGF活化的HIF-1α的稳定性。 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。

公开(公告)号：US06800479B2

公开(公告)日：2004-10-05

申请号：US10105080

申请日：2002-03-22

申请人： Dong-Soo Im ,  Won-Kyung Cho ,  Kyung-Sun Hwang

发明人： Dong-Soo Im ,  Won-Kyung Cho ,  Kyung-Sun Hwang

IPC分类号： C12N1524

CPC分类号： C07K14/54 ,  A61K48/00 ,  C12N2799/022

摘要： The present invention relates to recombinant adenoviruses expressing interleukin-18 protein, and gene therapy using them. More particularly, the invention provides recombinant adenoviruses Ad.promIL-18, Ad.GMmIL-18, Ad.prohIL-18, Ad.hIL-18CPP32- and Ad.preprotrypsin.hIL-18CPP32- which are effectively capable of treating a variety of cancer cells by promoting and enhancing an immune response in vivo.

摘要翻译： 本发明涉及表达白细胞介素-18蛋白的重组腺病毒，以及使用它们的基因治疗。 更具体地，本发明提供了重组腺病毒Ad.promIL-18，Ad.GMmIL-18，Ad.prohIL-18，Ad.hIL-18CPP32-和Ad.preprotrypsin.hIL-18CPP32-，它们有效地处理各种 癌细胞通过在体内促进和增强免疫应答。