Cell entry by SARS-CoV-2.

Cell entry by SARS-CoV-2.
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通过SARS-COV-2进入细胞。

DOI:
10.1016/j.tibs.2021.06.001
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发表时间:
2021-10
影响因子:
13.8
通讯作者:
Gao GF
Gao GF
中科院分区:
生物学1区
文献类型:
--
作者:
Peng R;Wu LA;Wang Q;Qi J;Gao GF

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严重急性呼吸综合征病毒2型(SARS-CoV-2)通过其刺突蛋白(S)与受体/辅助受体以及其他辅因子相互作用侵入宿主细胞,所述刺突蛋白进一步介导病毒和细胞膜之间的融合。宿主膜蛋白血管紧张素转换酶2(ACE 2)是SARS-CoV-2的主要受体,是跨物种传播的关键决定因素。此外,一些辅助受体和辅因子也参与了SARS-CoV-2的宿主/组织嗜性的扩展。受体结合后,需要特异性蛋白酶切割S蛋白并触发其融合活性。在这里,我们讨论了最近的进展,了解分子事件在SARS冠状病毒-2进入,这将有助于开发疫苗和治疗。
Severe acute respiratory syndrome virus 2 (SARS-CoV-2) invades host cells by interacting with receptors/coreceptors, as well as with other cofactors, via its spike (S) protein that further mediates fusion between viral and cellular membranes. The host membrane protein, angiotensin-converting enzyme 2 (ACE2), is the major receptor for SARS-CoV-2 and is a crucial determinant for cross-species transmission. In addition, some auxiliary receptors and cofactors are also involved that expand the host/tissue tropism of SARS-CoV-2. After receptor engagement, specific proteases are required that cleave the S protein and trigger its fusogenic activity. Here we discuss the recent advances in understanding the molecular events during SARS-CoV-2 entry which will contribute to developing vaccines and therapeutics.
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发表时间: 2020-11-13
期刊: Science (New York, N.Y.)
影响因子: --
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