ArticleJournal of virology2005
Shutoff of RNA polymerase II transcription by poliovirus involves 3C protease-mediated cleavage of the TATA-binding protein at an alternative site: incomplete shutoff of transcription interferes with efficient viral replication.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- Article
- A Proximity biotinylation assay with a host protein bait reveals multiple factors modulating enterovirus replication.PLoS pathogens · 2022Article
- Innate immune evasion mediated by picornaviral 3C protease: Possible lessons for coronaviral 3C-like protease?Reviews in medical virology · 2021Review
- The SARS-CoV-2 SSHHPS Recognized by the Papain-like Protease.ACS infectious diseases · 2021Article
- The Nuclear Pore Complex Is a Key Target of Viral Proteases to Promote Viral Replication.Viruses · 2021Review
- Critical Involvement of TFIIB in Viral Pathogenesis.Frontiers in molecular biosciences · 2021Review
- In vivo antiviral host transcriptional response to SARS-CoV-2 by viral load, sex, and age.PLoS biology · 2020Article
- Structural Biology of the Enterovirus Replication-Linked 5'-Cloverleaf RNA and Associated Virus Proteins.Microbiology and molecular biology reviews : MMBR · 2020Review
- Biochemical characterization of recombinant Avihepatovirus 3C protease and its localization.Virology journal · 2019Article
- Proteolytic cleavage of host proteins by the Group IV viral proteases of Venezuelan equine encephalitis virus and Zika virus.Antiviral research · 2019Article
- Calicivirus RNA-Dependent RNA Polymerases: Evolution, Structure, Protein Dynamics, and Function.Frontiers in microbiology · 2019Review
- Influenza virus infection causes global RNAPII termination defects.Nature structural & molecular biology · 2018Article
- Human Rhinovirus 3C protease cleaves RIPK1, concurrent with caspase 8 activation.Scientific reports · 2018Article
- Characterization of the African Swine Fever Virus Decapping Enzyme during Infection.Journal of virology · 2017Article
- A Novel Enterovirus 71 (EV71) Virulence Determinant: The 69th Residue of 3C Protease Modulates Pathogenicity.Frontiers in cellular and infection microbiology · 2017Article
- N-Terminal Domain of Feline Calicivirus (FCV) Proteinase-Polymerase Contributes to the Inhibition of Host Cell Transcription.Viruses · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The TATA-binding protein (TBP) plays a crucial role in cellular transcription catalyzed by all three DNA-dependent RNA polymerases. Previous studies have shown that TBP is targeted by the poliovirus (PV)-encoded protease 3C(pro) to bring about shutoff of cellular RNA polymerase II-mediated transcription in PV-infected cells. The processing of the majority of viral precursor proteins by 3C(pro) involves cleavages at glutamine-glycine (Q-G) sites. We present evidence that suggests that the transcriptional inactivation of TBP by 3C(pro) involves cleavage at the glutamine 104-serine 105 (Q104-S105) site of TBP and not at the Q18-G19 site as previously thought. The TBP Q104-S105 cleavage by 3C(pro) is greatly influenced by the presence of an aliphatic amino acid at the P4 position, a hallmark of 3C(pro)-mediated proteolysis. To examine the importance of host cell transcription shutoff in the PV life cycle, stable HeLa cell lines were created that express recombinant TBP resistant to cleavage by the viral proteases, called GG rTBP. Transcription shutoff was significantly impaired and delayed in GG rTBP cells upon infection with poliovirus compared with the cells that express wild-type recombinant TBP (wt rTBP). Infection of GG rTBP cells with poliovirus resulted in small plaques, significantly reduced viral RNA synthesis, and lower viral yields compared to the wt rTBP cell line. These results suggest that a defect in transcription shutoff can lead to inefficient replication of poliovirus in cultured cells.
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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.