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首页> 外文期刊>Biochemistry >Accumulating evidence suggests that several AB-toxins subvert the endoplasmic reticulum-associated protein degradation pathway to enter target cells
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Accumulating evidence suggests that several AB-toxins subvert the endoplasmic reticulum-associated protein degradation pathway to enter target cells

机译：越来越多的证据表明，几种AB毒素破坏了内质网相关蛋白的降解途径，使其进入靶细胞

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摘要

Several AB-toxins appear to have independently evolved mechanisms by which they undergo retrograde transport from the cell membrane to the endoplasmic reticulum (ER). Recent insights into ER-associated protein degradation (ERAD) now provide clues as to why these toxins have selected the ER as the site of cell entry. We propose that they disguise themselves as misfolded proteins to enter the ERAD pathway. We further link the observation that these toxins have few, if any, lysine residues to the need to escape ubiquitin-mediated protein degradation, the ultimate destination of the ERAD pathway. The actual membrane translocation step remains unclear, but studies on viral immune evasion mechanisms indicate that retrotranslocation across the ER lipid bilayer may involve SEC61. Understanding the internalization process of these toxins opens new avenues for preventing their entry into cells. In addition, this knowledge can be exploited to create protein-based pharmaceuticals that act on cytosolic targets.
机译：几种AB毒素似乎具有独立进化的机制，使它们经历从细胞膜到内质网（ER）的逆行转运。现在对ER相关蛋白降解（ERAD）的最新见解提供了有关这些毒素为何选择ER作为细胞进入位点的线索。我们建议他们伪装成错误折叠的蛋白质，以进入ERAD途径。我们进一步将这些毒素几乎没有赖氨酸残基的观察结果与逃避泛素介导的蛋白质降解（ERAD途径的最终目的地）的需要联系起来。实际的膜易位步骤尚不清楚，但是对病毒免疫逃逸机制的研究表明，跨过ER脂质双分子层的逆向易位可能涉及SEC61。了解这些毒素的内在化过程为防止其进入细胞开辟了新途径。此外，可以利用这些知识来创建对细胞溶质靶标起作用的基于蛋白质的药物。

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