鼠冠状病毒刺突蛋白的S2亚基不参与受体结合。
The S2 subunit of the murine coronavirus spike protein is not involved in receptor binding.
作者信息
Taguchi F
机构信息
National Institute of Neuroscience, NCNP, Tokyo, Japan.
出版信息
J Virol. 1995 Nov;69(11):7260-3. doi: 10.1128/JVI.69.11.7260-7263.1995.
Abstract
The receptor-binding capacity of the S2 subunit of the murine coronavirus S protein was examined by testing the inhibition of virus-receptor binding. Sp-4 virus and S1N(330), which consists of the N-terminal 330 amino acids of the S1 protein, both of which exhibited receptor-binding capacity, were able to prevent the binding of cl-2 virus to the receptor, while the mutant protein S1N(330)-159, which failed to bind to the receptor protein, and S2TM-, which lacks the transmembrane and cytoplasmic domains normally existing in the S2, were unable to prevent the binding of cl-2. By using cultured DBT cells, it was revealed that the infection of cells by cl-2 virus was significantly inhibited by S1N(330) but not by S2TM-. These results indicate that the S2 protein is not involved in the receptor binding of murine coronaviruses.
摘要
通过检测病毒-受体结合的抑制情况，研究了鼠冠状病毒S蛋白S2亚基的受体结合能力。Sp-4病毒和由S1蛋白N端330个氨基酸组成的S1N(330)，二者均表现出受体结合能力，能够阻止cl-2病毒与受体的结合，而未能与受体蛋白结合的突变蛋白S1N(330)-159以及缺少S2中正常存在的跨膜和胞质结构域的S2TM-，均无法阻止cl-2的结合。利用培养的DBT细胞发现，S1N(330)可显著抑制cl-2病毒对细胞的感染，而S2TM-则无此作用。这些结果表明，S2蛋白不参与鼠冠状病毒的受体结合。
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