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Viral immune modulators perturb the human molecular network by common and unique strategiesmRNA export through an additional cap-binding complex consisting of NCBP1 and NCBP3La Crosse Bunyavirus Nonstructural Protein NSs Serves To Suppress the Type I Interferon System of Mammalian HostsProcessing of Genome 5′ Termini as a Strategy of Negative-Strand RNA Viruses to Avoid RIG-I-Dependent Interferon InductionIncoming RNA virus nucleocapsids containing a 5'-triphosphorylated genome activate RIG-I and antiviral signalingInterferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activationSequestration by IFIT1 impairs translation of 2'O-unmethylated capped RNA.Ribose 2'-O-methylation provides a molecular signature for the distinction of self and non-self mRNA dependent on the RNA sensor Mda5.High-Throughput Screening Using a Whole-Cell Virus Replication Reporter Gene Assay to Identify Inhibitory Compounds against Rift Valley Fever Virus Infection.Early endonuclease-mediated evasion of RNA sensing ensures efficient coronavirus replicationVirulence factor NSs of rift valley fever virus recruits the F-box protein FBXO3 to degrade subunit p62 of general transcription factor TFIIHCytoplasmic sensing of viral nucleic acids.TMPRSS2 activates the human coronavirus 229E for cathepsin-independent host cell entry and is expressed in viral target cells in the respiratory epithelium.NSs protein of rift valley fever virus induces the specific degradation of the double-stranded RNA-dependent protein kinase.ISG56/IFIT1 is primarily responsible for interferon-induced changes to patterns of parainfluenza virus type 5 transcription and protein synthesisToscana virus induces interferon although its NSs protein reveals antagonistic activity.Virus-like particles expressing the nucleocapsid gene as an efficient vaccine against Rift Valley fever virus.Species-independent bioassay for sensitive quantification of antiviral type I interferons.Efficient production of Rift Valley fever virus-like particles: The antiviral protein MxA can inhibit primary transcription of bunyaviruses.T7 RNA polymerase-dependent and -independent systems for cDNA-based rescue of Rift Valley fever virus.Structure of human IFIT1 with capped RNA reveals adaptable mRNA binding and mechanisms for sensing N1 and N2 ribose 2'-O methylations.Vaccination with virus-like particles protects mice from lethal infection of Rift Valley Fever Virus.
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description
hulumtues
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Matthias Habjan
@ast
Matthias Habjan
@en
Matthias Habjan
@es
Matthias Habjan
@nl
Matthias Habjan
@sl
type
label
Matthias Habjan
@ast
Matthias Habjan
@en
Matthias Habjan
@es
Matthias Habjan
@nl
Matthias Habjan
@sl
prefLabel
Matthias Habjan
@ast
Matthias Habjan
@en
Matthias Habjan
@es
Matthias Habjan
@nl
Matthias Habjan
@sl
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P1153
24331236100
P21
P31
P496
0000-0002-3623-4496