ArticleEMBO reports2022
Dysregulation of the miR-30c/DLL4 axis by circHIPK3 is essential for KSHV lytic replication.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- The dynamic interplay between viruses and host non-coding RNA species.FEMS microbiology reviews · 2026Review
- Manipulation of Nuclear-Related Pathways During Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Viruses · 2025Review
- Pseudouridine prevalence in Kaposi's sarcoma-associated herpesvirus transcriptome reveals an essential mechanism for viral replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Article
- Virus-modified paraspeckle-like condensates are hubs for viral RNA processing and their formation drives genomic instability.Nature communications · 2024Article
- Imaging and quantification of human and viral circular RNAs.Nucleic acids research · 2024Article
- Interferon induced circRNAs escape herpesvirus host shutoff and suppress lytic infection.EMBO reports · 2024Article
- KSHV promotes oncogenic FOS to inhibit nuclease AEN and transactivate RGS2 for AKT phosphorylation.bioRxiv : the preprint server for biology · 2024Article
- mViruses · 2023Article
- Kaposi's sarcoma-associated herpesvirus induces specialised ribosomes to efficiently translate viral lytic mRNAs.Nature communications · 2023Article
- Dysregulation of the miR-30c/DLL4 axis by circHIPK3 is essential for KSHV lytic replication.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-coding RNA (ncRNA) regulatory networks are emerging as critical regulators of gene expression. These intricate networks of ncRNA:ncRNA interactions modulate multiple cellular pathways and impact the development and progression of multiple diseases. Herpesviruses, including Kaposi's sarcoma-associated herpesvirus, are adept at utilising ncRNAs, encoding their own as well as dysregulating host ncRNAs to modulate virus gene expression and the host response to infection. Research has mainly focused on unidirectional ncRNA-mediated regulation of target protein-coding transcripts; however, we identify a novel host ncRNA regulatory network essential for KSHV lytic replication in B cells. KSHV-mediated upregulation of the host cell circRNA, circHIPK3, is a key component of this network, functioning as a competing endogenous RNA of miR-30c, leading to increased levels of the miR-30c target, DLL4. Dysregulation of this network highlights a novel mechanism of cell cycle control during KSHV lytic replication in B cells. Importantly, disruption at any point within this novel ncRNA regulatory network has a detrimental effect on KSHV lytic replication, highlighting the essential nature of this network and potential for therapeutic intervention.
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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.