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1. 发明申请

WO2004027376A3 ASSAY FOR PPAR LIGAND DEPENDENT GENE MODULATION 审中-公开
标题翻译：测定PPAR配体依赖基因调控
公开(公告)号：WO2004027376A3
公开(公告)日：2005-04-14
申请号：PCT/US0328961
申请日：2003-09-16
申请人： SQUIBB BRISTOL MYERS CO , MUKHERJEE RANJAN , LIU PHILLIP , HUBER REID M , BURN TIMOTHY C , YOUNG PETER R
发明人： MUKHERJEE RANJAN , LIU PHILLIP , HUBER REID M , BURN TIMOTHY C , YOUNG PETER R
IPC分类号： C12Q1/68 , C07H21/04
CPC分类号： C12Q1/6897 , C12Q1/6883 , C12Q2600/158 , C12Q2545/107
摘要： The peroxisome proliferator activated receptor alpha (PPARalpha) plays a key role in mediating fatty acid metabolism by regulating expression of genes involved in fatty acid oxidation. A limitation of existing human cell models for testing PPARalpha ligands is the inability to detect PPAR responsive genes with endogenous levels of PPARalpha protein. The HK-2 cell line derived from human proximal tubules showed induction of several genes, including pyruvate dehydrogenase kinase 4 (PDK-4) and adipocyte differentiation related factor (ADRP) by PPARalpha ligands. Induction of PDK-4 by PPARalpha agonists in the HK-2 cell model closely correlates with its induction in vivo and thus represents a marker for PPARalpha agonist action. HK2 cells also exemplify the first model of a human cell line in which PPARalpha ligand dependent gene induction can be detected with endogenous levels of receptor.
摘要翻译：过氧化物酶体增殖物激活受体α（PPARα）通过调节参与脂肪酸氧化的基因的表达在调节脂肪酸代谢中起关键作用。用于测试PPARα配体的现有人类细胞模型的局限性是不能检测具有PPARα蛋白内源水平的PPAR应答基因。衍生自人近端小管的HK-2细胞系显示PPARα配体诱导几种基因，包括丙酮酸脱氢酶激酶4（PDK-4）和脂肪细胞分化相关因子（ADRP）。 HK-2细胞模型中PPARα激动剂对PDK-4的诱导与体内诱导密切相关，因此代表PPARα激动剂作用的标志物。 HK2细胞也体现了人类细胞系的第一种模式，其中可以用内源性受体水平检测PPARα配体依赖性基因诱导。

2. 发明申请

WO2004089294A2 COMPOSITIONS, METHODS AND KITS RELATING TO HER-2 CLEAVAGE 审中-公开
标题翻译：组合物，方法和与2-CLEAVAGE相关的试剂盒
公开(公告)号：WO2004089294A2
公开(公告)日：2004-10-21
申请号：PCT/US2004010278
申请日：2004-04-02
申请人： INCYTE CORP , FRIEDMAN STEVEN M , SCHERLE PEGGY A , LIU XIANGDONG , BURN TIMOTHY C , HUBER REID , LIU PHILLIP C C , HOLLIS GREGORY F , VADDI KRISHNA , FRIDMAN JORDAN S
发明人： FRIEDMAN STEVEN M , SCHERLE PEGGY A , LIU XIANGDONG , BURN TIMOTHY C , HUBER REID , LIU PHILLIP C C , HOLLIS GREGORY F , VADDI KRISHNA , FRIDMAN JORDAN S
IPC分类号： A61K20060101 , A61K31/19 , A61K39/395 , A61K
CPC分类号： A61K31/19 , A61K31/395
摘要： The present invention relates to compositions, methods and kits based on the ADAM-mediated cleavage of Her-2. The present invention also relates to treatments for cancer, and in particular, breast cancer, by modulating the ADAMmediated cleavage of Her-2. Further, the invention relates to compositions, methods and kits based on the surprising synergistic effect between inhibition of Her-2 cleavage by an ADAM and certain cytostatic (e.g., Herceptin) and cytotoxic (e.g., Taxol) compounds in, among other things, inhibiting tumor cell proliferation and inducing cell death. Additionally, the invention relates to novel variants of ADAM15, designated ADAM15 variant I and ADAM 15 variant 2, now identified and isolated.
摘要翻译：本发明涉及基于ADAM介导的Her-2切割的组合物，方法和试剂盒。本发明还涉及通过调节ADAM介导的Her-2切割来治疗癌症，特别是乳腺癌。此外，本发明涉及基于由ADAM抑制Her-2切割和某些细胞抑制（例如赫赛汀）和细胞毒性（例如紫杉醇）化合物之间令人惊讶的协同效应的组合物，方法和试剂盒，其中除其他外，抑制肿瘤细胞增殖和诱导细胞死亡。另外，本发明涉及现在鉴定和分离的ADAM15的新型变体，称为ADAM15变体I和ADAM 15变体2。

3. 发明申请

WO2004089294A3 COMPOSITIONS, METHODS AND KITS RELATING TO HER-2 CLEAVAGE 审中-公开
公开(公告)号：WO2004089294A3
公开(公告)日：2004-10-21
申请号：PCT/US2004/010278
申请日：2004-04-02
申请人： INCYTE CORPORATION , FRIEDMAN, Steven, M. , SCHERLE, Peggy, A. , LIU, Xiangdong , BURN, Timothy, C. , HUBER, Reid , LIU, Phillip, C., C. , HOLLIS, Gregory, F. , VADDI, Krishna , FRIDMAN, Jordan, S.
发明人： FRIEDMAN, Steven, M. , SCHERLE, Peggy, A. , LIU, Xiangdong , BURN, Timothy, C. , HUBER, Reid , LIU, Phillip, C., C. , HOLLIS, Gregory, F. , VADDI, Krishna , FRIDMAN, Jordan, S.
IPC分类号： A61K39/395 , A61K31/19
摘要： The present invention relates to compositions, methods and kits based on the ADAM-mediated cleavage of Her-2. The present invention also relates to treatments for cancer, and in particular, breast cancer, by modulating the ADAMmediated cleavage of Her-2. Further, the invention relates to compositions, methods and kits based on the surprising synergistic effect between inhibition of Her-2 cleavage by an ADAM and certain cytostatic (e.g., Herceptin) and cytotoxic (e.g., Taxol) compounds in, among other things, inhibiting tumor cell proliferation and inducing cell death. Additionally, the invention relates to novel variants of ADAM15, designated ADAM15 variant I and ADAM 15 variant 2, now identified and isolated.

4. 发明申请

WO2004027376A2 ASSAY FOR PPAR LIGAND DEPENDENT GENE MODULATION 审中-公开
标题翻译：测定PPAR配体依赖基因调控
公开(公告)号：WO2004027376A2
公开(公告)日：2004-04-01
申请号：PCT/US2003/028961
申请日：2003-09-16
申请人： BRISTOL-MYERS SQUIBB COMPANY , MUKHERJEE, Ranjan , LIU, Phillip , HUBER, Reid, M. , BURN, Timothy, C. , YOUNG, Peter, R.
发明人： MUKHERJEE, Ranjan , LIU, Phillip , HUBER, Reid, M. , BURN, Timothy, C. , YOUNG, Peter, R.
IPC分类号： G01N
CPC分类号： C12Q1/6897 , C12Q1/6883 , C12Q2600/158 , C12Q2545/107
摘要： The peroxisome proliferator activated receptor alpha (PPARα) plays a key role in mediating fatty acid metabolism by regulating expression of genes involved in fatty acid oxidation. A limitation of existing human cell models for testing PPARα ligands is the inability to detect PPAR responsive genes with endogenous levels of PPARα protein. The HK-2 cell line derived from human proximal tubules showed induction of several genes, including pyruvate dehydrogenase kinase 4 (PDK-4) and adipocyte differentiation related factor (ADRP) by PPARα ligands. Induction of PDK-4 by PPARα agonists in the HK-2 cell model closely correlates with its induction in vivo and thus represents a marker for PPARα agonist action. HK2 cells also exemplify the first model of a human cell line in which PPARα ligand dependent gene induction can be detected with endogenous levels of receptor.
摘要翻译：过氧化物酶体增殖物激活受体α（PPARα）通过调节参与脂肪酸氧化的基因的表达在调节脂肪酸代谢中起关键作用。用于测试PPARα配体的现有人类细胞模型的局限性是不能检测具有PPARα蛋白内源水平的PPAR应答基因。衍生自人近端小管的HK-2细胞系显示PPARα配体诱导几种基因，包括丙酮酸脱氢酶激酶4（PDK-4）和脂肪细胞分化相关因子（ADRP）。 HK-2细胞模型中PPARα激动剂对PDK-4的诱导与体内诱导密切相关，因此代表PPARα激动剂作用的标志物。 HK2细胞也体现了人类细胞系的第一种模式，其中可以用内源性受体水平检测PPARα配体依赖性基因诱导。

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