Fusion-defective mutants of mouse hepatitis virus A59 contain a mutation in the spike protein cleavage signal.
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Mechanisms of coronavirus cell entry mediated by the viral spike proteinThe Coronavirus Spike Protein Is a Class I Virus Fusion Protein: Structural and Functional Characterization of the Fusion Core ComplexEpisodic evolution mediates interspecies transfer of a murine coronavirusMurine Coronavirus Mouse Hepatitis Virus Is Recognized by MDA5 and Induces Type I Interferon in Brain Macrophages/MicrogliaCleavage of the SARS coronavirus spike glycoprotein by airway proteases enhances virus entry into human bronchial epithelial cells in vitro.Endoproteolytic processing of the ebola virus envelope glycoprotein: cleavage is not required for function.Pathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.Intracellular complexes of viral spike and cellular receptor accumulate during cytopathic murine coronavirus infections.Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism.Identification and characterization of the putative fusion peptide of the severe acute respiratory syndrome-associated coronavirus spike proteinMurine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.Contributions of the viral genetic background and a single amino acid substitution in an immunodominant CD8+ T-cell epitope to murine coronavirus neurovirulence.Coronaviruses induce entry-independent, continuous macropinocytosisEvaluation of SSYA10-001 as a replication inhibitor of severe acute respiratory syndrome, mouse hepatitis, and Middle East respiratory syndrome coronaviruses.Murine AKAP7 has a 2',5'-phosphodiesterase domain that can complement an inactive murine coronavirus ns2 gene.Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus.Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice.Cell-type-specific type I interferon antagonism influences organ tropism of murine coronavirusCoronavirus cell entry occurs through the endo-/lysosomal pathway in a proteolysis-dependent manner.The nsp1, nsp13, and M proteins contribute to the hepatotropism of murine coronavirus JHM.WU.Effects of an epitope-specific CD8+ T-cell response on murine coronavirus central nervous system disease: protection from virus replication and antigen spread and selection of epitope escape mutants.Persistent infection of cultured cells with mouse hepatitis virus (MHV) results from the epigenetic expression of the MHV receptor.Molecular anatomy of mouse hepatitis virus persistence: coevolution of increased host cell resistance and virus virulence.Analysis of a recombinant mouse hepatitis virus expressing a foreign gene reveals a novel aspect of coronavirus transcriptionInhibition of the alpha/beta interferon response by mouse hepatitis virus at multiple levels.Ready, set, fuse! The coronavirus spike protein and acquisition of fusion competenceSuppression subtractive hybridization method for the identification of a new strain of murine hepatitis virus from xenografted SCID mice.Activation of RNase L by Murine Coronavirus in Myeloid Cells Is Dependent on Basal Oas Gene Expression and Independent of Virus-Induced InterferonMiddle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation.Cell-type-specific activation of the oligoadenylate synthetase-RNase L pathway by a murine coronavirus.Homologous 2',5'-phosphodiesterases from disparate RNA viruses antagonize antiviral innate immunity.Organ-specific attenuation of murine hepatitis virus strain A59 by replacement of catalytic residues in the putative viral cyclic phosphodiesterase ns2.Antagonism of RNase L Is Required for Murine Coronavirus Replication in Kupffer Cells and Liver Sinusoidal Endothelial Cells but Not in Hepatocytes.The N-terminal domain of the murine coronavirus spike glycoprotein determines the CEACAM1 receptor specificity of the virus strain.Lineage A Betacoronavirus NS2 Proteins and the Homologous Torovirus Berne pp1a Carboxy-Terminal Domain Are Phosphodiesterases That Antagonize Activation of RNase L.Identification and characterization of a proteolytically primed form of the murine coronavirus spike proteins after fusion with the target cell.Persistent infection of human oligodendrocytic and neuroglial cell lines by human coronavirus 229E.Acute and persistent infection of human neural cell lines by human coronavirus OC43.Ebola virus glycoprotein: proteolytic processing, acylation, cell tropism, and detection of neutralizing antibodiesThe spike protein of murine coronavirus mouse hepatitis virus strain A59 is not cleaved in primary glial cells and primary hepatocytes.
P2860
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P2860
Fusion-defective mutants of mouse hepatitis virus A59 contain a mutation in the spike protein cleavage signal.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
1993年论文
@zh
1993年论文
@zh-cn
name
Fusion-defective mutants of mo ...... spike protein cleavage signal.
@en
type
label
Fusion-defective mutants of mo ...... spike protein cleavage signal.
@en
prefLabel
Fusion-defective mutants of mo ...... spike protein cleavage signal.
@en
P2093
P2860
P1433
P1476
Fusion-defective mutants of mo ...... spike protein cleavage signal.
@en
P2093
J L Gombold
S T Hingley
P2860
P304
P407
P577
1993-08-01T00:00:00Z