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    • 3. 发明授权
    • Virion-based fusion assay
    • 基于Virion的融合测定
    • US07250251B2
    • 2007-07-31
    • US10656803
    • 2003-09-04
    • Warner C. GreeneMarielle CavroisCarlos de Noronha
    • Warner C. GreeneMarielle CavroisCarlos de Noronha
    • C12Q1/70
    • C07K14/005C07K2319/00C12N7/00C12N2740/16322C12Q1/6897
    • The present invention features methods and compositions relating to a virion-based fusion assay for detection of infection of a target cell by an enveloped retroviral virion such as HIV. The assay uses virions containing a chimeric viral protein comprising a viral accessory polypeptide (such as Vpr) fused to a reporter polypeptide (such as beta-lactamase). Fusion of the virion with a target cell membrane results in intracellular delivery of the chimeric protein to the target cell, which in turn provides for detection of a detectable signal mediated by the reporter polypeptide portion of the chimeric polypeptide. Significant detectable signal is only detected following intracellular delivery of the chimeric viral protein, thus providing for detection of productive viral entry to the exclusion of non-productive, endocytic entry of virions into the cell.
    • 本发明的特征在于与基于病毒体的融合测定相关的方法和组合物,用于通过包膜的逆转录病毒药物(例如HIV)检测靶细胞的感染。 该测定使用含有嵌合病毒蛋白质的病毒体,其包含与报道多肽(例如β-内酰胺酶)融合的病毒辅助多肽(例如Vpr)。 病毒粒子与靶细胞膜的融合导致嵌合蛋白质的细胞内递送至靶细胞,其又提供检测由嵌合多肽的报道多肽部分介导的可检测信号。 仅在嵌合病毒蛋白质的细胞内递送后才检测到显着的可检测信号,从而提供检测生产性病毒进入以排除病毒体进入细胞的非生产性内吞进入。
    • 10. 发明授权
    • Inhibitor of the inflammatory response induced by the TNFA and IL-1
    • 由TNFA和IL-1诱导的炎症反应的抑制剂
    • US06265538B1
    • 2001-07-24
    • US09257703
    • 1999-02-25
    • Warner C. GreeneXin LinRomas Gelezuinas
    • Warner C. GreeneXin LinRomas Gelezuinas
    • A61K3800
    • C12N9/1205
    • The present invention provides the molecular basis for cytokine induction of NF-&kgr;B-dependent immune and inflammatory responses, emphasizing a role for both NIK-NIK and NIK-IKK protein-protein interactions. A relatively small region of NIK selectively impairs the NIK-IKK interaction. The present invention provides a highly specific method for modulating NF-&kgr;B-dependent immune, inflammatory, and anti-apoptotic responses, based on interruption of the critical protein-protein interaction of NIK and IKK. The present invention provides methods for inhibiting NF-&kgr;B-dependent gene expression, using mutant NIK proteins. One embodiment of the present invention provides kinase-deficient NIK mutant proteins that inhibit activation of IKK. Another embodiment of the invention provides N-terminus NIK mutant proteins that bind IKK, thus inhibiting NIK/IKK interaction.
    • 本发明提供NF-κB依赖性免疫和炎症反应的细胞因子诱导的分子基础,强调NIK-NIK和NIK-IKK蛋白质 - 蛋白质相互作用的作用。 NIK相对较小的区域选择性地损害NIK-IKK相互作用。 本发明基于NIK和IKK的关键蛋白质 - 蛋白质相互作用的中断,提供了调节NF-κB依赖性免疫,炎症和抗凋亡反应的高度特异性方法。 本发明提供使用突变NIK蛋白抑制NF-κB依赖性基因表达的方法。 本发明的一个实施方案提供抑制IKK活化的激酶缺陷型NIK突变蛋白。 本发明的另一个实施方案提供结合IKK的N末端NIK突变蛋白,从而抑制NIK / IKK相互作用。