Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The PA-X host shutoff site 100 V exerts a contrary effect on viral fitness of the highly pathogenic H7N9 influenza A virus in mice and chickens

28 Dec 2024

Abstract excerpt

Several viruses, including influenza A virus (IAV), encode viral factors to hijack cellular RNA biogenesis processes to direct the degradation of host mRNAs, termed "host shutoff." Host shutoff enables viruses to simultaneously reduce antiviral responses and provides preferential access for viral mRNAs to cellular translation machinery. IAV PA-X is one of these factors that selectively shuts off the global host...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Influenza Virus Research Studies
Share to interferon and immune responses
Share to Respiratory viral infections research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39731774
DOI: 10.1080/21505594.2024.2445238

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The PA-X host shutoff site 100 V exerts a contrary effect on viral fitness of the highly pathogenic H7N9 influenza A virus in mice and chickensPMID 39731774Read ↗

PA-X I94V mutation modulates the pathogenicity of the highly pathogenic H7N9 influenza A virus in mice and chickens.Semantic proximity Read ↗

Specificity and functional interplay between influenza virus PA-X and NS1 shutoff activitySemantic proximity Read ↗

Influenza A Virus Protein PA-X Contributes to Viral Growth and Suppression of the Host Antiviral and Immune ResponsesSemantic proximity Read ↗

Influenza A virus NS1 effector domain is required for PA-X-mediated host shutoff in infected cellsSemantic proximity Read ↗

Impaired host shutoff is a fitness cost associated with baloxavir marboxil resistance mutations in influenza A virus PA/PA-X nuclease domainSemantic proximity Read ↗

Impaired host shutoff is a fitness cost associated with baloxavir marboxil resistance mutations in influenza A virus PA/PA-X nuclease domain.Semantic proximity Read ↗

Influenza A virus NS1 effector domain is required for PA-X mediated host shutoffSemantic proximity Read ↗

PA-X: a key regulator of influenza A virus pathogenicity and host immune responsesSemantic proximity Read ↗

Critical Role of the PA-X C-Terminal Domain of Influenza A Virus in Its Subcellular Localization and Shutoff Activity.Semantic proximity Read ↗

Impacts of different expressions of PA-X protein on 2009 pandemic H1N1 virus replication, pathogenicity and host immune responses.Semantic proximity Read ↗

N-terminal acetylation controls multiple functional aspects of the influenza A virus ribonuclease PA-XSemantic proximity Read ↗

PA and PA-X: two key proteins from segment 3 of the influenza virusesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.