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    Method of detecting effect of controlling synoviolin activity
    1.
    发明申请
    Method of detecting effect of controlling synoviolin activity 审中-公开
    检测滑膜炎活性影响的方法

    公开(公告)号：US20070134720A1

    公开(公告)日：2007-06-14

    申请号：US10568913

    申请日：2004-08-20

    申请人： Toshihiro Nakajima ,  Tetsuya Amano ,  Lei Zhang ,  Rie Ikeda ,  Satoshi Yamasaki ,  Naoko Yagishita ,  Hiromitsu Yokohama ,  Motoji Kogushi

    发明人： Toshihiro Nakajima ,  Tetsuya Amano ,  Lei Zhang ,  Rie Ikeda ,  Satoshi Yamasaki ,  Naoko Yagishita ,  Hiromitsu Yokohama ,  Motoji Kogushi

    IPC分类号： A61K38/48 ,  G01N33/53 ,  C12Q1/37

    CPC分类号： A61K38/16 ,  A61K38/005 ,  C12Q1/25 ,  C12Q1/26 ,  G01N2333/90245 ,  G01N2500/00

    摘要： The present invention provides methods for evaluating the regulation on prolyl 4-hydroxylase activity. The present invention also provides screening methods using the evaluation methods. Furthermore, the present invention provides methods of screening for compounds that are useful for treating or preventing fibrosis or rheumatoid arthritis. The present invention relates to methods for detecting regulatory activity on the synoviolin ubiquitination of prolyl 4-hydroxylase α subunit (P4HA1). It also relates to methods of screening for compounds with regulatory effect on the ubiquitination activity of synoviolin on P4HA1 based on these methods. Compounds discovered in the screening are useful for treating and/or preventing diseases caused by abnormalities in the prolyl 4-hydroxylase activity, such as fibrosis and rheumatoid arthritis.

    摘要翻译： 本发明提供了评估脯氨酰4-羟化酶活性调节的方法。 本发明还提供了使用评价方法的筛选方法。 此外，本发明提供筛选可用于治疗或预防纤维化或类风湿性关节炎的化合物的方法。 本发明涉及检测脯氨酰4-羟化酶α亚基（P4HA1）的滑膜蛋白泛素化的调节活性的方法。 它还涉及基于这些方法筛选对P4HA1上滑膜素泛素化活性具有调节作用的化合物的方法。 在筛选中发现的化合物可用于治疗和/或预防由脯氨酰4-羟化酶活性异常引起的疾病，例如纤维化和类风湿性关节炎。

    Promoter of Synoviolin Gene
    6.
    发明申请
    Promoter of Synoviolin Gene 审中-公开
    滑膜蛋白基因启动子

    公开(公告)号：US20080070298A1

    公开(公告)日：2008-03-20

    申请号：US10569330

    申请日：2004-08-23

    申请人： Toshihiro Nakajima ,  Tetsuya Amano ,  Satoshi Yamasaki ,  Naoko Yagishita ,  Kaneyuki Tsuchimochi

    发明人： Toshihiro Nakajima ,  Tetsuya Amano ,  Satoshi Yamasaki ,  Naoko Yagishita ,  Kaneyuki Tsuchimochi

    IPC分类号： C12N5/10 ,  C07H21/00 ,  C12N1/00 ,  C12N15/63

    CPC分类号： C07K14/47

    摘要： The present invention provides a promoter of the synoviolin gene comprising at least the nucleotide sequence of nucleotides 2120-2130 in the nucleotide sequence represented by SEQ ID: NO 1 or 2, or comprising at least the nucleotide sequence of the region of nucleotides 1-2201, 969-2201, 1142-2201, 1699-2201, 1880-2201, 2002-2201, 2094-2201 or 2118-2201 in the nucleotide sequence represented by SEQ ID: NO 1 or 2;or a method for regulating transcription activity characterized in that the activity of the promoter is inhibited or enhanced.

    摘要翻译： 本发明提供滑膜蛋白基因的启动子，其至少包含由SEQ ID NO：1所示的核苷酸序列中的核苷酸2120-2130的核苷酸序列，或者至少包含核苷酸区域的核苷酸序列1-2201 ，969-2201,1142-2201,1699-2201,1880-2201,2002-2201,2094-2201或2118-2201所示的核苷酸序列;或调节转录活性的方法，其特征在于 因为启动子的活性被抑制或增强。

    Protein formulations comprising s1-5
    9.
    发明申请
    Protein formulations comprising s1-5 审中-公开
    包含s1-5的蛋白质​​制剂

    公开(公告)号：US20090276863A1

    公开(公告)日：2009-11-05

    申请号：US11631040

    申请日：2005-07-01

    申请人： Toshihiro Nakajima ,  Naoko Yagishita ,  Tetsuya Amano

    发明人： Toshihiro Nakajima ,  Naoko Yagishita ,  Tetsuya Amano

    IPC分类号： A61K49/00 ,  A01K67/027 ,  C12N5/10 ,  C12N15/09 ,  G01N33/567 ,  G01N33/00 ,  C07K14/00 ,  A61K38/16 ,  C07K16/00 ,  A61P35/00

    CPC分类号： C07K14/475 ,  A01K67/0276 ,  A01K2217/075 ,  A01K2227/105 ,  A01K2267/035 ,  A61K38/00 ,  G01N33/5044

    摘要： The present inventors discovered that knockout mice whose S1-5 gene function is lost develop age-related diseases or symptoms. Histological analysis in such knockout mice revealed that bone mineral content, bone mineral density, and bone strength were decreased, and the number of osteoclasts in bone tissues was increased. Analysis of osteoclast-forming ability using bone marrow cells derived from the knockout mice revealed that osteoclast-forming ability is enhanced and osteoclasts are larger in the knockout mice than in wildtype mice. When purified S1-5 protein was added to this in vitro system, osteoclast-forming ability was inhibited.

    摘要翻译： 本发明人发现S1-5基因功能丧失的敲除小鼠发生与年龄相关的疾病或症状。 在这种敲除小鼠中的组织学分析显示，骨矿物质含量，骨矿物质密度和骨强度降低，骨组织中破骨细胞数量增加。 使用衍生自敲除小鼠的骨髓细胞破骨细胞形成能力的分析显示，在野生型小鼠中，敲除小鼠的破骨细胞形成能力增强，破骨细胞较大。 当纯化的S1-5蛋白加入体外时，破骨细胞形成能力受到抑制。

    PROTEIN FORMULATIONS COMPRISING S1-5
    10.
    发明申请
    PROTEIN FORMULATIONS COMPRISING S1-5 审中-公开
    包含S1-5的蛋白质​​制剂

    公开(公告)号：US20100058488A1

    公开(公告)日：2010-03-04

    申请号：US11994327

    申请日：2005-12-28

    申请人： Toshihiro Nakajima ,  Naoko Yagishita ,  Tetsuya Amano

    发明人： Toshihiro Nakajima ,  Naoko Yagishita ,  Tetsuya Amano

    IPC分类号： A01K67/033 ,  C12N5/078 ,  C12N5/071 ,  A01K67/00 ,  G01N33/53 ,  C07K14/00 ,  C07K2/00 ,  A61K38/16 ,  C07K16/00 ,  A61P35/00 ,  A61P25/28

    CPC分类号： C07K14/47 ,  A01K67/027 ,  A01K67/0276 ,  A01K2217/075 ,  A01K2227/105 ,  A01K2267/03 ,  A01K2267/0368 ,  A61K38/00 ,  C12N15/8509

    摘要： The present inventors discovered that knockout mice whose S1-5 gene function is lost develop age-related diseases or symptoms. In such knockout mice, bone mineral content, bone mineral density, and bone strength were found to be decreased, and the number of osteoclasts in bone tissues was found to be increased. Analysis of osteoclast-forming ability using bone marrow cells derived from the knockout mice revealed that osteoclast-forming ability is enhanced and osteoclasts are larger in the knockout mice than in wildtype mice. When purified S1-5 protein was added to this in vitro system, osteoclast-forming ability was inhibited. Furthermore, administration of purified S1-5 protein to osteoporotic model mice showed that this protein has the effect of improving osteoporosis. The above findings demonstrate that S1-5 protein is useful for treating and preventing age-related diseases such as osteoporosis.

    摘要翻译： 本发明人发现S1-5基因功能丧失的敲除小鼠发生与年龄相关的疾病或症状。 在这样的敲除小鼠中，发现骨矿物质含量，骨矿物质密度和骨强度降低，并且发现骨组织中破骨细胞的数量增加。 使用衍生自敲除小鼠的骨髓细胞破骨细胞形成能力的分析显示，在野生型小鼠中，敲除小鼠的破骨细胞形成能力增强，破骨细胞较大。 当纯化的S1-5蛋白加入体外时，破骨细胞形成能力受到抑制。 此外，将纯化的S1-5蛋白施用于骨质疏松模型小鼠显示该蛋白质具有改善骨质疏松症的作用。 以上研究结果表明，S1-5蛋白可用于治疗和预防年龄相关疾病如骨质疏松症。