ArticleEMBO reports2023
CCR4-NOT differentially controls host versus virus poly(a)-tail length and regulates HCMV infection.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Selective decay of interferon mRNAs controls antiviral immunity and innate memory.Molecular cell · 2026Article
- Extended poly(A) tails are a shared feature of herpesvirus mRNAs.PLoS pathogens · 2026Article
- Stress Granule Sequestration of CCR4-NOT Promotes Poly(A) Lengthening of Stress-Survival Transcripts.bioRxiv : the preprint server for biology · 2026Article
- Review
- Extended poly(A) tails are a shared feature of herpesvirus mRNAs.bioRxiv : the preprint server for biology · 2025Article
- Nanopore guided annotation of transcriptome architectures.mSystems · 2024Article
- Nanopore Guided Annotation of Transcriptome Architectures.bioRxiv : the preprint server for biology · 2024Article
- CCR4-NOT differentially controls host versus virus poly(a)-tail length and regulates HCMV infection.EMBO reports · 2023Article
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 5 institutions in 3 countries.
Funding
Abstract
Unlike most RNA and DNA viruses that broadly stimulate mRNA decay and interfere with host gene expression, human cytomegalovirus (HCMV) extensively remodels the host translatome without producing an mRNA decay enzyme. By performing a targeted loss-of-function screen in primary human fibroblasts, we here identify the host CCR4-NOT deadenylase complex members CNOT1 and CNOT3 as unexpected pro-viral host factors that selectively regulate HCMV reproduction. We find that the scaffold subunit CNOT1 is specifically required for late viral gene expression and genome-wide host responses in CCR4-NOT-disrupted cells. By profiling poly(A)-tail lengths of individual HCMV and host mRNAs using nanopore direct RNA sequencing, we reveal poly(A)-tails of viral messages to be markedly longer than those of cellular mRNAs and significantly less sensitive to CCR4-NOT disruption. Our data establish that mRNA deadenylation by host CCR4-NOT is critical for productive HCMV replication and define a new mechanism whereby herpesvirus infection subverts cellular mRNA metabolism to remodel the gene expression landscape of the infected cell. Moreover, we expose an unanticipated host factor with potential to become a therapeutic anti-HCMV target.
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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.