MUC1, caspase-8, and DED-containing proteins
    1.
    发明授权
    MUC1, caspase-8, and DED-containing proteins 有权
    MUC1,caspase-8和含DED蛋白

    公开(公告)号:US08809002B2

    公开(公告)日:2014-08-19

    申请号:US13003539

    申请日:2009-07-09

    Applicant: Donald W. Kufe

    Inventor: Donald W. Kufe

    Abstract: The disclosure features a variety of compositions and methods for modulating an interaction between MUC1 and caspase-8 and/or an interaction between MUC1 and a DED-containing protein (e.g., an anti-apoptotic DED-containing protein or a pro-apoptotic DED-containing protein). Such methods and compositions are useful for the treatment or prevention of e.g., a variety of pathological disorders characterized by elevated or decreased levels of apoptosis. Moreover, the compositions and methods are also useful to identify, design, and generate compounds that modulate the interactions. The compounds and/or pharmaceutical compositions containing the compounds can be used in the treatment of disease.

    Abstract translation: 该公开内容特征在于用于调节MUC1和半胱天冬酶-8之间的相互作用和/或MUC1与含DED的蛋白质之间的相互作用的多种组合物和方法(例如,含抗凋亡DED的蛋白质或促凋亡DED- 含蛋白质)。 这些方法和组合物可用于治疗或预防例如以细胞凋亡水平升高或降低为特征的各种病理学疾病。 此外,组合物和方法也可用于鉴定,设计和产生调节相互作用的化合物。 含有这些化合物的化合物和/或药物组合物可用于治疗疾病。

    Methods and compositions relating to the regulation of apoptosis by MUC1 and BH3-containing proapoptotic proteins
    4.
    发明授权
    Methods and compositions relating to the regulation of apoptosis by MUC1 and BH3-containing proapoptotic proteins 有权
    与通过MUC1和含BH3的促凋亡蛋白调节凋亡相关的方法和组合物

    公开(公告)号:US07871784B2

    公开(公告)日:2011-01-18

    申请号:US12024715

    申请日:2008-02-01

    Applicant: Donald W. Kufe

    Inventor: Donald W. Kufe

    CPC classification number: C07K14/4747 G01N2500/02 G01N2500/10

    Abstract: This invention relates to regulation of cell signaling, cell growth, and more particularly to the regulation of cancer or immune cell growth. The invention provides methods of inhibiting interactions between MUC1 and BH3-containing proapoptotic proteins, methods of inhibiting MUC1 expression, and methods of promoting apoptosis. Also provided are screening methods for compounds that inhibit interactions between MUC1 and BH3-containing proapoptotic proteins and pharmaceutical compositions of the same.

    Abstract translation: 本发明涉及细胞信号调节,细胞生长,更具体地涉及癌细胞或免疫细胞生长的调控。 本发明提供了抑制含有MUC1和含BH3的促凋亡蛋白之间相互作用的方法,抑制MUC1表达的方法以及促进细胞凋亡的方法。 还提供抑制含有MUC1和含BH3的促凋亡蛋白之间相互作用的化合物及其药物组合物的筛选方法。

    Constitutive gene expression in conjuction with ionizing radiation
    6.
    发明授权
    Constitutive gene expression in conjuction with ionizing radiation 失效
    与电离辐射结合的组成型基因表达

    公开(公告)号:US07592317B1

    公开(公告)日:2009-09-22

    申请号:US08289290

    申请日:1994-08-11

    CPC classification number: A61K48/005 C12N2799/022

    Abstract: The present disclosure demonstrates the successful use of constitutive promoters operatively linked to genes encoding radiosensitizing or radioprotecting factors, administered to cells, tissues, or patients in conjunction with radiation exposure. Also disclosed are pharmacological preparations to be used to increase the levels of radiosensitizing compounds such as TNF-α, or radioprotective compounds such as MnSOD, in specified tissues or tumors of a subject.

    Abstract translation: 本公开内容显示了与辐射照射联合施用于细胞,组织或患者的与编码放射增敏剂或放射防护因子的基因有效连接的组成型启动子的成功应用。 还公开了用于在受试者的特定组织或肿瘤中增加放射增敏化合物如TNF-α或放射防护化合物如MnSOD的药理学制剂。

    Regulation of x-ray mediated gene expression
    7.
    发明授权
    Regulation of x-ray mediated gene expression 失效
    调节X线介导的基因表达

    公开(公告)号:US5641755A

    公开(公告)日:1997-06-24

    申请号:US278452

    申请日:1994-07-20

    CPC classification number: A61K31/40 A61K31/70 A61K41/0019 A61K41/0023

    Abstract: Treatment of cells with ionizing radiation is associated with the production of arachidonic acid. Inhibition of phospholipase A2 abolishes radiation-mediated arachidonate production, protein kinase C induction and tumor necrosis factor gene expression. The addition of inhibitors of lipoxygenase, such as ketoconazole, prior to irradiation reduces the expression of of tumor necrosis factor while maintaining the expression of other radiation inducible genes, such as Egr-1 and c-jun. In contrast, indomethacin, an inhibitor of cyclooxygenase, enhanced the expression of tumor necrosis factor as well as other radiation inducible genes. The results show that lipoxygenase inhibitors are useful in the treatment of radiation-induced mucositis, dermatitis, pneumonitis, proctitis, and esophagitis. which may be due to the production of cytokines such as TNF.

    Abstract translation: 用电离辐射处理细胞与花生四烯酸的生产有关。 磷脂酶A2的抑制消除辐射介导的花生四烯酸生成,蛋白激酶C诱导和肿瘤坏死因子基因表达。 在照射之前加入脂氧合酶抑制剂如酮康唑可降低肿瘤坏死因子的表达,同时保持其他放射诱导基因如Egr-1和c-jun的表达。 相比之下,吲哚美辛是环氧合酶抑制剂,增强了肿瘤坏死因子以及其他辐射诱导基因的表达。 结果表明,脂氧合酶抑制剂可用于治疗放射诱导的粘膜炎,皮炎,肺炎,直肠炎和食道炎。 这可能是由于产生诸如TNF的细胞因子。

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