ArticleCell host & microbe2013
Type I interferon imposes a TSG101/ISG15 checkpoint at the Golgi for glycoprotein trafficking during influenza virus infection.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- Organelle-centered ISG15 biology: distinguishing covalent ISGylation from interferon-associated responses.Frontiers in immunology · 2026Review
- Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs.Pathogens (Basel, Switzerland) · 2024Review
- Usp25-Erlin1/2 activity limits cholesterol flux to restrict virus infection.Developmental cell · 2023Article
- Adaptive design of mRNA-loaded extracellular vesicles for targeted immunotherapy of cancer.Nature communications · 2023Article
- Viral subversion of selective autophagy is critical for biogenesis of virus replication organelles.Nature communications · 2023Article
- Hepatitis B virus hijacks TSG101 to facilitate egress via multiple vesicle bodies.PLoS pathogens · 2023Article
- The HIV Restriction Factor Profile in the Brain Is Associated with the Clinical Status and Viral Quantities.Viruses · 2023Article
- Interferon-stimulated gene 15 facilitates BTV replication through interacting with the NS1 protein.Frontiers in microbiology · 2023Article
- Free ISG15 Inhibits the Replication of Peste des Petits Ruminants Virus by Breaking the Interaction of Nucleoprotein and Phosphoprotein.Microbiology spectrum · 2022Article
- PSMD12-Mediated M1 Ubiquitination of Influenza A Virus at K102 Regulates Viral Replication.Journal of virology · 2022Article
- A diminished immune response underlies age-related SARS-CoV-2 pathologies.Cell reports · 2022Article
- Tumor Susceptibility Gene 101 (TSG101) Contributes to Virion Formation of Porcine Reproductive and Respiratory Syndrome Virus via Interaction with the Nucleocapsid (N) Protein along with the Early Secretory Pathway.Journal of virology · 2022Article
- Identification of Nifurtimox and Chrysin as Anti-Influenza Virus Agents by Clinical Transcriptome Signature Reversion.International journal of molecular sciences · 2022Article
- Application of the CRISPR/Cas9 System to Study Regulation Pathways of the Cellular Immune Response to Influenza Virus.Viruses · 2022Review
- Roles of ESCRT Proteins ALIX and CHMP4A and Their Interplay with Interferon-Stimulated Gene 15 during Tick-Borne Flavivirus Infection.Journal of virology · 2022Article
- Altered ISGylation drives aberrant macrophage-dependent immune responses during SARS-CoV-2 infection.Nature immunology · 2021Article
- The ESCRT-I Subunit Tsg101 Plays Novel Dual Roles in Entry and Replication of Classical Swine Fever Virus.Journal of virology · 2021Article
- The Role of Post-Translational Modifications in Targeting Protein Cargo to Extracellular Vesicles.Sub-cellular biochemistry · 2021Article
- Potential Molecular Mechanisms and Remdesivir Treatment for Acute Respiratory Syndrome Corona Virus 2 Infection/COVID 19 Through RNA Sequencing and Bioinformatics Analysis.Bioinformatics and biology insights · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Several enveloped viruses exploit host pathways, such as the cellular endosomal sorting complex required for transport (ESCRT) machinery, for their assembly and release. The influenza A virus (IAV) matrix protein binds to the ESCRT-I complex, although the involvement of early ESCRT proteins such as Tsg101 in IAV trafficking remain to be established. We find that Tsg101 can facilitate IAV trafficking, but this is effectively restricted by the interferon (IFN)-stimulated protein ISG15. Cytosol from type I IFN-treated cells abolished IAV hemagglutinin (HA) transport to the cell surface in infected semi-intact cells. This inhibition required Tsg101 and could be relieved with deISGylases. Tsg101 is itself ISGylated in IFN-treated cells. Upon infection, intact Tsg101-deficient cells obtained by CRISPR-Cas9 genome editing were defective in the surface display of HA and for infectious virion release. These data support the IFN-induced generation of a Tsg101- and ISG15-dependent checkpoint in the secretory pathway that compromises influenza virus release.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.