别名 F、F1、F2 + [8] |
简介 Class I viral fusion protein (PubMed:23618766). Under the current model, the protein has at least 3 conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state (PubMed:23618766). During viral and plasma cell membrane fusion, the coiled coil regions assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain (PubMed:19966279, PubMed:23618766). The formation of this structure appears to drive apposition and subsequent fusion of viral and cellular membranes leading to delivery of the nucleocapsid into the cytoplasm (PubMed:23593008, PubMed:23618766). This fusion is pH independent and occurs at the plasma or endosomal membrane (Probable). The trimer of F1-F2 (F protein) also facilitates the attachment to host cell by binding to host heparan sulfate (PubMed:10864656). F protein is involved in the entry into the host cell through the interaction with host IGF1R (PubMed:32494007). This interaction activates PRKCZ/PKCzeta that recruits host NCL/nucleolin to the apical cell surface where it can bind fusion glycoprotein F1 (PubMed:21841784, PubMed:32494007). Later in infection, F protein expressed at the plasma membrane of infected cells can mediate fusion with adjacent cells to form syncytia, a cytopathic effect that could lead to tissue necrosis (PubMed:10438814). F protein may trigger p53-dependent apoptosis (PubMed:18216092).
Major determinant of the species specificity of RSV infection (PubMed:12663767). The trimer of F1-F2 (F protein) also facilitates the attachment to host cell by binding to host heparan sulfate (PubMed:10864656). F protein is involved in the entry into the host cell through the interaction with host IGF1R (PubMed:32494007). This interaction activates PRKCZ/PKCzeta that recruits host NCL/nucleolin to the apical cell surface where it can bind fusion glycoprotein F1 (PubMed:32494007). Later in infection, F protein expressed at the plasma membrane of infected cells can mediate fusion with adjacent cells to form syncytia, a cytopathic effect that could lead to tissue necrosis (PubMed:10438814). F protein seems to trigger p53-dependent apoptosis (PubMed:18216092).
Inactive precursor that is cleaved at two sites by a furin-like protease to give rise to the mature F1 and F2 fusion glycoproteins. |
作用机制 Respiratory syncytial virus F protein调节剂 |
在研机构 |
原研机构 |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批国家/地区 欧盟 [+3] |
首次获批日期2024-08-22 |
作用机制 Respiratory syncytial virus F protein调节剂 |
在研机构 |
原研机构 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批国家/地区 加拿大 |
首次获批日期2023-01-04 |
作用机制 呼吸道合胞病毒F蛋白抑制剂 |
原研机构 |
在研适应症 |
非在研适应症- |
最高研发阶段批准上市 |
首次获批国家/地区 欧盟 [+3] |
首次获批日期2022-10-31 |
开始日期2025-04-30 |
申办/合作机构 |
开始日期2025-04-16 |
申办/合作机构 |
开始日期2025-04-04 |
申办/合作机构 |