Anti-Respiratory Syncytial Virus Fusion (F) Glycoprotein 抗体 [RSV3216 (B016)]

靶点信息

Fusion glycoprotein F0. Inactive precursor that is cleaved at two sites by a furin-like protease to give rise to the mature F1 and F2 fusion glycoproteins.. Fusion glycoprotein F1. 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).. Fusion glycoprotein F2. 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).