Methods and compositions for providing cardiac protection
    31.
    发明授权
    Methods and compositions for providing cardiac protection 有权
    提供心脏保护的方法和组合物

    公开(公告)号:US08871735B2

    公开(公告)日:2014-10-28

    申请号:US13668897

    申请日:2012-11-05

    CPC classification number: A61K31/7076

    Abstract: The invention provides a method of reducing infarct size and/or limiting, decreasing and/or inhibiting reperfusion injury and/or ameliorating heart failure in a patient comprising administering a pharmaceutically effective amount of at least one compound capable of inhibiting AC5 to the patient. The compound capable of inhibiting AC5 is particularly effective when administered during or after reperfusion in patients suffering from an ischemic injury.

    Abstract translation: 本发明提供了一种降低梗死面积和/或限制,减少和/或抑制患者的再灌注损伤和/或改善心力衰竭的方法,包括向患者施用药学有效量的至少一种能够抑制AC5的化合物。 能够抑制AC5的化合物在再灌注期间或之后在患有缺血性损伤的患者中施用时特别有效。

    Site-specific protein modification
    39.
    发明申请
    Site-specific protein modification 失效
    位点特异性蛋白质修饰

    公开(公告)号:US20020106767A1

    公开(公告)日:2002-08-08

    申请号:US09972016

    申请日:2001-10-04

    Abstract: Site-specific modified proteins and method for producing site-specific modified proteins using amino acid analogs are disclosed. Methods for labeling proteins at a desired site in the presence of nucleophilic side chains, including lysine and cysteine side chains, are also disclosed. Methods for labeling the site-specific modified proteins are also disclosed.

    Abstract translation: 公开了位点特异性修饰蛋白质和使用氨基酸类似物产生位点特异性修饰蛋白质的方法。 还公开了在亲核侧链(包括赖氨酸和半胱氨酸侧链)存在下在所需位点标记蛋白质的方法。 还公开了用于标记位点特异性修饰蛋白质的方法。

    MRNA Interferase from Myxococcus Xanthus
    40.
    发明申请
    MRNA Interferase from Myxococcus Xanthus 审中-公开
    来自Myxococcus Xanthus的MRNA干扰酶

    公开(公告)号:US20140193878A1

    公开(公告)日:2014-07-10

    申请号:US13932498

    申请日:2013-07-01

    CPC classification number: C12N9/16 C07K14/195

    Abstract: A regulated deployment of a toxin gene for developmental programmed cell death in bacteria is described. M. xanthus is demonstrated to have a solitary mazF gene that lacks a cotranscribed antitoxin gene. Deletion of mazF results in elimination of the obligatory cell death during development causing dramatic reduction in spore formation. Surprisingly, MrpC functions as a MazF antitoxin and a mazF transcription activator. Transcription of mrpC and mazF is negatively regulated via MrpC phosphorylation by a Ser/Thr kinase cascade. Various methods of exploiting this novel pathway are described herein.

    Abstract translation: 描述了在细菌中发育程序性细胞死亡的毒素基因的调节性部署。 黄曲霉被证明具有缺乏共转录的抗毒素基因的孤立的mazF基因。 mazF的删除导致在发育过程中消除强制性细胞死亡,导致孢子形成的显着减少。 令人惊讶的是,MrpC起MazF抗毒素和mazF转录激活物的作用。 mrpC和mazF的转录通过Ser / Thr激酶级联的MrpC磷酸化负调控。 本文描述了利用这种新途径的各种方法。

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