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1 antagonize HIV-1 Env at gp120 V1V2 to block viral membrane fusion.
2 disordered (ld) phase boundary to facilitate viral membrane fusion.
3 mbrane ordering is a common prerequisite for viral membrane fusion.
4 ntagonists blocked infection at the level of viral membrane fusion.
5 on at a postendocytic entry step, presumably viral membrane fusion.
6 , thereby lowering the activation energy for viral membrane fusion.
7 iochemical understanding of low-pH-triggered viral membrane fusion.
8 ral role for the N-terminal glycine ridge in viral membrane fusion.
9 the plasma membrane being less permissive to viral membrane fusion.
10 -2 spike (S) protein and thus interfere with viral membrane fusion.
11 cular basis for an improved understanding of viral membrane fusion.
12 e activation of the F protein and inhibiting viral membrane fusion.
13 ing cells, where LY6E predominantly promotes viral membrane fusion.
14 st-attachment stage, with several inhibiting viral membrane fusion.
16 ngs provide new fundamental understanding of viral membrane fusion and are relevant to structure-guid
18 irus envelope, supports the current model of viral membrane fusion and gives insight into the design
19 l glycoprotein 2 (GP2) which facilitate host-viral membrane fusion and subsequent release of the vira
21 idual mutations in the three proteins of the viral membrane fusion apparatus, M, fusion (F), and hema
23 is required to facilitate the triggering of viral membrane fusion by destabilizing the prefusion con
24 onance analysis suggested that 10E8 inhibits viral membrane fusion by lifting the MPER N-terminal reg
25 vides an overview of the basic principles of viral membrane fusion common to all enveloped viruses an
27 lical coiled-coil core relates gB to class I viral membrane fusion glycoproteins; two extended beta h
28 fusion potential of influenza HA, like many viral membrane-fusion glycoproteins, is generated by pro
29 osomal compartment are probably required for viral membrane fusion; however, despite considerable eff
30 ors and altered endosomal trafficking affect viral membrane fusion.IMPORTANCE Many enveloped viruses
31 e, which is transiently exposed during HIV-1 viral membrane fusion, is a validated clinical target in
32 ) and L (gL) comprise a basal element of the viral membrane fusion machinery conserved across herpesv
33 oop, a critical and conserved element of the viral membrane fusion machinery, and neutralize viral en
35 M structure of Atlas G(C) reveals a class II viral membrane fusion protein fold not previously seen i
36 nucleopolyhedrovirus (AcMNPV) is a class III viral membrane fusion protein that is triggered by low p
38 (FAST) proteins comprise a unique family of viral membrane fusion proteins dedicated to inducing cel
43 ity after PRV infection due to the action of viral membrane fusion proteins, yet it is unclear if suc
45 ved prehairpin intermediate (PHI) of class I viral membrane-fusion proteins are generally weakly neut
46 ved prehairpin intermediate (PHI) of class I viral membrane-fusion proteins typically show limited ne
47 that the coiled-coil motif occurs in several viral membrane-fusion proteins, including HIV-1 gp41 and
48 overall architecture resembles several other viral membrane-fusion proteins, including those from HIV
51 ace loop at the cleavage site that activates viral membrane fusion reveal structural features primari
52 Despite their diversity, basic principles of viral membrane fusion, simultaneous engagement of both d
54 to a CoRA-dependent decrease in the rate of viral membrane fusion that extends the lifetime of the i
57 blocked productive infection at the level of viral membrane fusion, with a range of inhibitory activi