ArticleProceedings of the National Academy of Sciences of the United States of America2012
AAA ATPase p97/VCP is essential for TRIM21-mediated virus neutralization.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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
63 citing papers in PubMed, 103 citations in OpenAlex.
- Advances in Alzheimer's disease: mechanistic insights and therapeutic targets.Science China. Life sciences · 2026Review
- Cell-autonomous immunity as an integrated immune network against bacterial and viral pathogens.Nature microbiology · 2026Review
- Redirecting TRIM21 with TRIMTACs for the targeted degradation of multimeric proteins.The FEBS journal · 2026Review
- Systematic identification of tissue-conserved mbioRxiv : the preprint server for biology · 2026Article
- Host AAA-ATPase VCP/p97 lyses ubiquitinated intracellular bacteria as an innate antimicrobial defence.Nature microbiology · 2025Article
- Pulmonary Myeloid Cells in Mild Cases of COVID-19 Upregulate the Intracellular Fc ReceptorInternational journal of molecular sciences · 2025Article
- Immunological pathogenesis and treatment progress of adenovirus pneumonia in children.Italian journal of pediatrics · 2025Review
- Co-opting templated aggregation to degrade pathogenic tau assemblies and improve motor function.Cell · 2024Article
- Aggregate-selective removal of pathological tau by clustering-activated degraders.Science (New York, N.Y.) · 2024Article
- TRIM21 restricts influenza A virus replication by ubiquitination-dependent degradation of M1.PLoS pathogens · 2023Article
- Regulation of PKR-dependent RNA translation inhibition by TRIM21 upon virus infection or other stress.PLoS pathogens · 2023Article
- Multiple Roles of TRIM21 in Virus Infection.International journal of molecular sciences · 2023Review
- Functional skewing of TRIM21-SIRT5 interplay dictates IL-1β production in DSS-induced colitis.EMBO reports · 2022Article
- Comparative analysis of ChAdOx1 nCoV-19 and Ad26.COV2.S SARS-CoV-2 vector vaccines.Haematologica · 2022Article
- Antibody bivalency improves antiviral efficacy by inhibiting virion release independently of Fc gamma receptors.Cell reports · 2022Article
- Restriction factor compendium for influenza A virus reveals a mechanism for evasion of autophagy.Nature microbiology · 2021Article
- Rab11-FIP1 and Rab11-FIP5 Regulate pIgR/pIgA Transcytosis through TRIM21-Mediated Polyubiquitination.International journal of molecular sciences · 2021Article
- How Viruses Use the VCP/p97 ATPase Molecular Machine.Viruses · 2021Review
- A functional assay for serum detection of antibodies against SARS-CoV-2 nucleoprotein.The EMBO journal · 2021Article
- Induced TRIM21 ISGylation by IFN-β enhances p62 ubiquitination to prevent its autophagosome targeting.Cell death & disease · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Tripartite motif-containing 21 (TRIM21) is a cytosolic IgG receptor that mediates intracellular virus neutralization by antibody. TRIM21 targets virions for destruction in the proteasome, but it is unclear how a substrate as large as a viral capsid is degraded. Here, we identify the ATPase p97/valosin-containing protein (VCP), an enzyme with segregase and unfoldase activity, as a key player in this process. Depletion or catalytic inhibition of VCP prevents capsid degradation and reduces neutralization. VCP is required concurrently with the proteasome, as addition of inhibitor after proteasomal degradation has no effect. Moreover, our results suggest that it is the challenging nature of virus as a substrate that necessitates involvement of VCP, since intracellularly expressed IgG Fc is degraded in a VCP-independent manner. These results implicate VCP as an important host factor in antiviral immunity.
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.