ArticleProceedings of the National Academy of Sciences of the United States of America2013
Pooled RNAi screen identifies ubiquitin ligase Itch as crucial for influenza A virus release from the endosome during virus entry.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.
- Meta- and Orthogonal Integration of Influenza "OMICs" Data Defines a Role for UBR4 in Virus Budding.Cell host & microbe · 2015Pooled it
- SARS-CoV-2 3CL protease interaction with host factors - identifying novel drug targets.Archives of virology · 2026Review
- Genome-Wide RNAi Screening Identifies Novel Host Factors Involved in Influenza A Virus Infection in A549 Cells.Viruses · 2026Article
- Influenza A virus subverts the LC3-pericentrin dynein adaptor complex for host cytoplasm entry.Science advances · 2025Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- CRISPR editing of candidate host factors that impact influenza A virus infection.Microbiology spectrum · 2025Article
- Understanding Influenza.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Profiling Cullin4-E3 Ligases Interactomes and Their Rewiring in Influenza A Virus Infection.Molecular & cellular proteomics : MCP · 2024Article
- HACD3 Prevents PB1 from Autophagic Degradation to Facilitate the Replication of Influenza A Virus.Viruses · 2024Article
- An evolutionarily conserved ubiquitin ligase drives infection and transmission of flaviviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- A disintegrin and metalloproteinase domain 9 facilitates SARS-CoV-2 entry into cells with low ACE2 expression.Microbiology spectrum · 2023Article
- Ubiquitin-Dependent and Independent Proteasomal Degradation in Host-Pathogen Interactions.Molecules (Basel, Switzerland) · 2023Review
- Host factor TNK2 is required for influenza virus infection.Genes & genomics · 2023Article
- Upregulation of galectin-3 in influenza A virus infection promotes viral RNA synthesis through its association with viral PA protein.Journal of biomedical science · 2023Article
- Nonmuscle myosin IIA promotes the internalization of influenza A virus and regulates viral polymerase activity through interacting with nucleoprotein in human pulmonary cells.Virologica Sinica · 2023Article
- Influenza A Virus: Cellular Entry.Sub-cellular biochemistry · 2023Article
- Cellular glycan modification by B3GAT1 broadly restricts influenza virus infection.Nature communications · 2022Article
- Article
- Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza viruses, like other viruses, rely on host factors to support their life cycle as viral proteins usually "hijack," or collaborate with, cellular proteins to execute their functions. Identification and understanding of these factors can increase the knowledge of molecular mechanisms manipulated by the viruses and facilitate development of antiviral drugs. To this end, we developed a unique genome-wide pooled shRNA screen to search for cellular factors important for influenza A virus (IAV) replication. We identified an E3 ubiquitin ligase, Itch, as an essential factor for an early step in the viral life cycle. In Itch knockdown cells, the incorporation of viral ribonucleoprotein complex into endosomes was normal, but its subsequent release from endosomes and transport to the nucleus was retarded. In addition, upon virus infection, Itch was phosphorylated and recruited to the endosomes, where virus particles were located. Furthermore, Itch interacted with viral M1 protein and ubiquitinated M1 protein. Collectively, our findings unravel a critical role of Itch in mediating IAV release from the endosome and offer insights into the mechanism for IAV uncoating during virus entry. These findings also highlight the feasibility of pooled RNAi screening for exploring the cellular cofactors of lytic viruses.
Indexed as
Identifiers
What OpenQuestion holds
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.