利索-全球专利检索

  1. 登录
  2. 注册

搜索结果

23 条记录 (耗时 0.03 秒)

    GLUCOSE-DEPENDENT INSULINOTROPIC PEPTIDE FOR USE AS AN OSTEOTROPIC HORMONE
    5.
    发明授权
    GLUCOSE-DEPENDENT INSULINOTROPIC PEPTIDE FOR USE AS AN OSTEOTROPIC HORMONE 有权
    葡萄糖依赖性，INSULINOTROPISCHES肽使用AS osteotropic激素

    公开(公告)号：EP1119625B1

    公开(公告)日：2005-06-29

    申请号：EP99950250.3

    申请日：1999-10-07

    申请人： Medical College Of Georgia Research Institute, Inc.

    发明人： ISALES, Carlos, M. ,  BOLLAG, Roni, J. ,  RASMUSSEN, Howard

    IPC分类号： C12N15/16 ,  C07K14/605 ,  C07K16/26 ,  A61K38/26 ,  A01K67/027 ,  A61P19/10

    CPC分类号： A01K67/0275 ,  A01K2217/05 ,  A01K2227/105 ,  A61K38/00 ,  C07K14/605

    摘要： The examples demonstrate that GIP receptor mRNA and protein are present in normal bone and osteoblastic-like cell lines, and that high-affinity receptors for GIP can be demonstrated by 125 I GIP binding studies. When applied to osteoblast-like cells (SaOS2), GIP stimulated an increase in cellular cAMP content and in intracellular calcium, with both responses being dose dependent. Moreover, administration of GIP results in elevated expression of collagen type I mRNA as well as an increase in alkaline phosphatase activity. Both of these effects reflect anabolic actions of presumptive osteoblasts. These results provide the first evidence that GIP receptors are present in bone and osteoblastic-like cells and that GIP modulates the function of these cells. GIP has anabolic actions on remodeling bone, increasing vertebral bone density in a rat model of osteoporosis. GIP at 10nM inhibits PTH-induced bone resorption in a fetal long bone assay and stimulates the synthesis of type 1 collagen mRNA. Transgenic mice overexpressing GIP have increased bone density compared to same age controls. GIP or analogs thereof can therefore be used as a therapeutic to inhibit bone resorption and to maintain or increase bone density. GIP antagonists, compounds which block binding to the GIP receptor, can be used to decrease bone density.

    D-1 LIKE DOPAMINE RECEPTOR ACTIVITY MODIFYING PROTEIN
    6.
    发明授权
    D-1 LIKE DOPAMINE RECEPTOR ACTIVITY MODIFYING PROTEIN 有权
    蛋白，其修饰D1-LIKE多巴胺受体的活性

    公开(公告)号：EP1117688B1

    公开(公告)日：2005-04-27

    申请号：EP99951895.4

    申请日：1999-10-08

    申请人： Medical College Of Georgia Research Institute, Inc.

    发明人： BERGSON, Clare

    IPC分类号： C07K14/47 ,  C12N15/12 ,  G01N33/68

    CPC分类号： C07K14/4702 ,  G01N33/9413 ,  G01N2500/00

    摘要： A number of cDNA clones whose products may interact with D1 receptors in vivo were identified. One of the clones, P24, was characterized further. P24 is localized in dendtrites and spines of pyramidal cells in PFC. The extent of overlap between P24 expressing and D1 receptor expressing pyramidal cells appeared to be 100 %. In contrast, only a limited number D1 receptor antibody labeled neurons in caudate expressed P24. P24 lowers the threshold of D1 receptor response to dopamine (DA) by an order of magnitude. Sequence similarity suggests P24 is a diverged member of the RAMP family. The P24 protein is therefore referred to as a D1 DA RAMP, calcyon. The isolated protein and nucleotide molecule encoding the protein, as well as primers for the nucleotide, are described. The protein and compounds modifying DA binding to the receptor or calcium release which is mediated by the Calcyon, are useful in research studies, drug screening, and therapeutically.

    BREAST CANCER SUSCEPTIBILITY GENE GT198 AND USES THEREOF
    7.
    发明公开
    BREAST CANCER SUSCEPTIBILITY GENE GT198 AND USES THEREOF 有权
    乳腺癌易感基因GT198及其用途

    公开(公告)号：EP2421991A1

    公开(公告)日：2012-02-29

    申请号：EP10719454.0

    申请日：2010-04-19

    申请人： Medical College Of Georgia Research Institute, Inc

    发明人： KO, Lan

    IPC分类号： C12Q1/68

    CPC分类号： C12Q1/6886 ,  C12Q2600/136 ,  C12Q2600/156 ,  C12Q2600/158

    摘要： It has been discovered that the human GT198 gene (gene symbol PSMC3IP) at chromosome 17q21 acts as a tumor suppressor. The mutation of the GT198 gene causes the increased dominant negative splice variant activity and leads to the loss of wild type GT198 function, and in turn, induces breast and ovarian cancers. One embodiment provides compositions and methods for treating or alleviating one or more symptoms associated with cancer due to the GT198 gene mutations. Another embodiment provides methods and compositions for detecting cancer due to the mutation of the GT198 gene. Still another embodiment provides methods for identifying compounds, antibodies and natural product molecules that are useful for treating cancer due to the mutations of the GT198 gene. Preferably the disclosed compositions antagonize or interfere with the biological activity of splice variants of GT198.