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    METHODS AND MATERIALS FOR MODULATING DEUBIQUITINASES AND UBIQUITINATED POLYPEPTIDES
    4.
    发明申请
    METHODS AND MATERIALS FOR MODULATING DEUBIQUITINASES AND UBIQUITINATED POLYPEPTIDES 审中-公开
    调节分子量和无定形多糖的方法和材料

    公开(公告)号：US20160136248A1

    公开(公告)日：2016-05-19

    申请号：US14956635

    申请日：2015-12-02

    Applicant: Mayo Foundation for Medical Education and Research

    Inventor： Zhenkun Lou ,  Jian Yuan

    IPC: A61K38/46

    CPC classification number: A61K38/46 ,  A61K31/7105 ,  A61K38/4873 ,  A61K38/55 ,  C12Q1/005 ,  C12Q1/37 ,  C12Y306/04012 ,  G01N33/5011 ,  G01N33/573 ,  G01N2333/4748 ,  G01N2333/81 ,  G01N2500/00 ,  G01N2500/02

    Abstract: This document relates to methods and materials involved in modulating deubiquitinases (e.g., USP10 polypeptides) and/or ubiquitinated polypeptides (e.g., tumor suppressor polypeptides or mutant versions of tumor suppressor polypeptides). For example, methods and materials for increasing deubiquitinase (e.g., a USP10 polypeptide) expression or activity, methods and materials for decreasing deubiquitinase (e.g., a USP10 polypeptide) expression or activity, methods and materials for stabilizing tumor suppressor polypeptides (e.g., wild-type p53 polypeptides), methods and materials for de-stabilizing mutant versions of tumor suppressor polypeptides (e.g., mutant p53 polypeptides), and methods and materials for reducing cancer cell proliferation, increasing cancer cell apoptosis, and/or treating cancer (e.g., cancers having reduced levels of wild-type p53 polypeptides or cancers having increased levels of mutant p53 polypeptides) are provided. This document also provides methods and materials for identifying agonists or antagonists of USP10 polypeptide mediated stabilization of p53 polypeptides.

    Abstract translation: 本文件涉及调节去泛素酶（例如，USP10多肽）和/或泛素化多肽（例如肿瘤抑制多肽或肿瘤抑制多肽的突变体形式）的方法和材料。 例如，用于增加去泛素化酶（例如，USP10多肽）表达或活性的方法和材料，用于降低去泛素酶（例如，USP10多肽）的表达或活性的方法和材料，用于稳定肿瘤抑制多肽的方法和材料（例如，野生型 - 类型p53多肽），用于去稳定肿瘤抑制多肽的突变型（例如，突变型p53多肽）的方法和材料，以及用于降低癌细胞增殖，增加癌细胞凋亡和/或治疗癌症（例如癌症）的方法和材料 提供具有降低水平的野生型p53多肽或具有增加的突变型p53多肽水平的癌症）。 本文件还提供了鉴定USP10多肽介导的p53多肽稳定化的激动剂或拮抗剂的方法和材料。

    "> BIO-ENGINEERED HYPER-FUNCTIONAL
    8.
    发明申请
    BIO-ENGINEERED HYPER-FUNCTIONAL "SUPER" HELICASES 审中-公开

    公开(公告)号：US20170335297A1

    公开(公告)日：2017-11-23

    申请号：US15526905

    申请日：2015-11-13

    Applicant: THE BOARD OF TRUSTEES OF THE UNIVERSITY OF ILLINOIS

    Inventor： Taekjip HA ,  Sinan ARSLAN

    IPC: C12N9/14 ,  C12P19/34

    CPC classification number: C12N9/14 ,  C12N9/90 ,  C12P19/34 ,  C12Y306/04012

    Abstract: Conformationally-constrained helicases having improved activity and strength are provided. Methods of making conformationally-constrained helicases having improved activity and strength are provided. Methods of using conformationally-constrained helicases having improved activity and strength are provided. The present invention is based on the discovery of novel modified helicases that show dramatically enhanced helicase activity and increased strength as compared to unmodified helicases. As described further herein, it has been surprisingly discovered that, by controlling the conformation of certain subdomains such that the helicase remains in a closed form (e.g., by covalently crosslinking the 2B domain to the 1A domain or the 1B domain in a Rep helicase), a highly active and strong form of the helicase is achieved

    INHIBITION OF DNA2 IN FANCONI ANEMIA
    10.
    发明申请
    INHIBITION OF DNA2 IN FANCONI ANEMIA 有权
    DNA2在FANCONI ANEMIA中的抑制作用

    公开(公告)号：US20150111950A1

    公开(公告)日：2015-04-23

    申请号：US14520318

    申请日：2014-10-21

    Applicant: California Institute of Technology

    Inventor： Kenneth Karanja ,  Martin E. Budd ,  Judith L. Campbell

    IPC: C12N15/113

    CPC classification number: C12N15/1137 ,  C12N2310/14 ,  C12N2320/31 ,  C12Y306/04012 ,  C12N2310/531

    Abstract: Inhibition of DNA2 in Fanconi anemia (FA) cells remedies the over-resection of DNA, thereby stabilizing the FA cells. Inhibition of DNA2 in FA cells allows for safe treatment of cancers in FA patients, a decrease in the lethality of FA cells, a decrease in bone marrow failure of FA patients, and a means for decreasing the incidence of cancer for FA patients.

    Abstract translation: 在Fanconi贫血（FA）细胞中DNA2的抑制补救了DNA的过度切除，从而稳定了FA细胞。 FA细胞中DNA2的抑制允许FA患者的癌症的安全治疗，FA细胞的致死性降低，FA患者的骨髓衰竭减少，以及降低FA患者的癌症发生率的方法。

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