LitCovid-sentences  

PMC:7074424 / 12349-17019 JSONTXT 15 Projects

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Id Subject Object Predicate Lexical cue
T87 0-13 Sentence denotes Spike protein
T88 14-373 Sentence denotes The spike protein is a clove-shaped, type I-TM protein.[2] The spike protein has three segments that are ectodomain (ED) region, TM region, and intracellular domain, which comprises the intracellular short tail part.[2] The receptor-binding S1 domain (three S1 heads) and the membrane fusion subunit S2 (trimeric stalk) on C-terminal together comprise the ED.
T89 374-1023 Sentence denotes Spike proteins gather in the trimeric form on the outer surface of the virion, giving it the appearance of a crown, due to which it is called CoV.[2] The spike protein plays an important role in virus entry into the host.[10] Initial interactions between the S1 domain and its host receptor (ACE2 in case of SARS-CoV and PP 4 In case of MERS-CoV) and subsequent S2 segment mediated fusion of the host and viral membranes allow the CoV- RNA genome to enter inside the host cells and thus, these proteins represent as important targets from drug discovery side.[10] The spike protein also activates the immune response of the host cell toward CoV.[10]
T90 1025-1034 Sentence denotes S1 domain
T91 1035-1136 Sentence denotes The main components of the S1 domain are the N-terminal domain (NTD) and the C-terminal domain (CTD).
T92 1137-1444 Sentence denotes The S1 domain acts as a major antigen on the surface of the virus[40] and has a receptor-binding domain (RBD).[25] The 18 residues of ACE-2 interact with the RBD (contain 14 amino acids) of SARS-CoV spike protein,[45] and for this contact, K341 of ACE-2 and R453 residue of RBD play the most important role.
T93 1445-1609 Sentence denotes If point mutated on the D454 or R441 of RBD, it disturbs the binding activity with ACE-2.[25] The S1 domain interacts with the ACE-2 or DPP-4 receptors of the host.
T94 1610-2078 Sentence denotes Anti-ACE-2 antibody blocked viral entry and replication in Vero E6 cells.[1445] One another mechanism of virus for binding to host cell is using dendritic cell-specific intercellular adhesion molecule-3 grabbing non-integrin (DC-SIGN receptor) or L-SIGN in lymph nodes or in liver.[4647] S protein has seven (109, 118, 119, 158, 227, 589, and 699) glycosylation asparagine-linked sites, which is pivotal for both L-SIGN- or DC-SIGN-based virus entry into the host.[48]
T95 2080-2090 Sentence denotes S2 subunit
T96 2091-2184 Sentence denotes The S2 subunit has two heptad repeat regions (HR 1 and 2) and hydrophobic fusion peptide.[25]
T97 2186-2252 Sentence denotes Drug designing strategies targeting S protein and its interactions
T98 2253-2488 Sentence denotes The RBD is targeted in many drug designing studies.[25] A peptide sequence with sequence similarity to the RBD of S protein hampered S1-RBD: ACE-2 interaction and prevented entry of SARS-CoV into Vero cells (IC50 around 40 μM).[254950]
T99 2489-2578 Sentence denotes A SARS-CoV RBD-specific antibody (FM6) failed to inhibit the occurrence of infection.[39]
T100 2579-2878 Sentence denotes OC43-HR2P, a peptide derived from heptad repeat 2 regions of S2 domain of HCoV-OC43 and its optimized form EK1, showed pan-CoV fusion inhibition property.[39] The structure (protein data bank [PDB] ID 5ZUV and 5ZVM) shows a stable 6-helix bundle structure with α-HCoV and long β-HCoV-HR1 domain.[39]
T101 2879-3074 Sentence denotes Chloroquine, an antimalarial agent, inhibits SERS-CoV by elevation of endosomal pH and alters the terminal glycosylation of ACE-2, which ultimately interferes with the virus receptor binding.[51]
T102 3075-3282 Sentence denotes Other inhibitors SSAA09E2 block the S-ACE2 interaction, SSAA09E1 inhibits the host protease cathepsin L (which is important for viral entry), and SSAA09E3 prevents fusion of host and viral cell membrane.[52]
T103 3283-3774 Sentence denotes Kao et al. identified 18 small molecules that targeted the S-ACE-2-mediated entry of virus into human cell.[53] In 293T cells expressing ACE-2, one of these agents (VE607) showed a significant inhibition of SARS-pseudovirus entry.[53] In Vero E6 cells, two other molecules tetra-O-galloyl beta-D-glucose and luteolin also inhibited SARS-pseudovirus and SARS-CoV infection.[53] In virus-infected Vero E6 cells, a siRNA against the S sequences of SARS-CoV inhibited SARS-CoV replication.[2554]
T104 3775-4026 Sentence denotes The S230 antibody (origin: memory B-cells of SARS-CoV-infected persons) neutralizes wide spectrum of isolates of SARS-CoV.[55] S230 antibody Fab fragment binds to the SARS-CoV complex to neutralize it, and their structures are also available (PDB IDs:
T105 4027-4131 Sentence denotes 6NB6, 6NB7, and 6NB8.[55] The monoclonal antibody, m396, has a competitive role for RBD binding (PDB ID:
T106 4132-4142 Sentence denotes 2DD8).[56]
T107 4143-4473 Sentence denotes Monoclonal antibody can be generated by immunizing the spike protein of SERS-CoV (transgenic mice) or from the B-cells of CoV-infected persons.[25] Spike-specific monoclonal antibodies 80R and CR301 block the S-ACE-2 interactions and thus neutralize infection by human SARS-CoV (HKu39849 and Tor2) and palm civet strain (SZ3).[25]
T108 4474-4670 Sentence denotes Mice vaccinated with SARS-n DNA showed T-cell immune response (both induction and proliferation),[57] and cytotoxic T-cell response was seen against SARS-DNA-transfected alveolar epithelial cells.