| 组氨酸质子化触发病毒膜融合及其分子机制 |
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| 引用本文： | 秦照玲,;鞠鹤鹏,;戚中田.组氨酸质子化触发病毒膜融合及其分子机制[J].生命的化学,2014(5):654-659. |
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| 作者姓名： | 秦照玲 ;鞠鹤鹏 ;戚中田 |
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| 作者单位： | [1]第二军医大学微生物学教研室、上海市医学生物防护重点实验室,上海200433; [2]广州军区疾病预防控制中心,广州510000 |
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| 基金项目： | 国家自然科学基金项目（30900066;81171564）;上海市重点学科建设项目（B901） |
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| 摘 要： | 膜融合是有包膜病毒入侵靶细胞的关键步骤,低pH、受体结合、二者兼具或其他尚未界定的机制均可触发病毒融合蛋白的构象重排,介导病毒包膜与靶细胞膜或内体膜间的融合。组氨酸(histidine,His)残基是唯一一个质子化状态变化(pKa~6~7)接近于病毒融合阈值(~pH6)的氨基酸,参与多种低pH依赖的病毒融合蛋白构象转变及膜融合,对其可能作用机制的阐述将有助于抗病毒药物的研制与发展。
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| 关 键 词： | 有包膜病毒 膜融合 组氨酸 质子化 低pH |
Virus member fusion triggered by histidine protonation and its molecular mechanism |
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| Institution: | QIN Zhaoling, JU Hepeng, QI Zhongtian(1 Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China; 2 Disease Prevention and Control Center of Guangzhou Military Region, Guangzhou 510000, China) |
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| Abstract: | Member fusion is a critical step of enveloped viruses to enter target cells. The fusion of viral en- velope with target cell membrane or endosomal membrane is mediated by viral fusion protein, whose confor- mational rearrangements can be triggered by low pH, receptor binding, both or other undefined mechanisms. Histidine （His） residue is believed to be involved in low pH- dependent conformational transitions of viral fusion proteins and subsequent member fusion since it is the only residue whose protonation state changes （pKa-6-7） is close to the fusion threshold of viruses at -pH6. The illustration of the possible mechanisms will contribute to the design and development of anti-viral drugs. |
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| Keywords: | enveloped viruses member fusion histidine protonation low pH |
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