ArticleScientific reports2017
Cleavage of poly(A)-binding protein by duck hepatitis A virus 3C protease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Duck hepatitis A virus 3CD and 3D proteins are key facilitators of hnRNP K expression and cytoplasmic entry, and hijack hnRNP K to facilitate viral translation and replication.Poultry science · 2025Article
- Canine parvovirus NS1 induces host translation shutoff by reducing mTOR phosphorylation.Journal of virology · 2025Article
- Duck hepatitis A virus utilizes PCBP2 to facilitate viral translation and replication.Veterinary research · 2024Article
- HSP70 positively regulates translation by interacting with the IRES and stabilizes the viral structural proteins VP1 and VP3 to facilitate duck hepatitis A virus type 1 replication.Veterinary research · 2024Article
- Molecular Detection and Genetic Characterization of Vertically Transmitted Viruses in Ducks.Animals : an open access journal from MDPI · 2023Article
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- DHAV 3CD targets IRF7 and RIG-I proteins to block the type I interferon upstream signaling pathway.Veterinary research · 2023Article
- The DHAV-1 protein VP1 interacts with PI3KC3 to induce autophagy through the PI3KC3 complex.Veterinary research · 2022Article
- Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase.Virology journal · 2022Article
- When Poly(A) Binding Proteins Meet Viral Infections, Including SARS-CoV-2.Journal of virology · 2022Review
- Article
- Attenuated Duck Hepatitis A Virus Infection Is Associated With High mRNA Maintenance in Duckling LiverFrontiers in immunology · 2022Article
- Innate immune evasion mediated by picornaviral 3C protease: Possible lessons for coronaviral 3C-like protease?Reviews in medical virology · 2021Review
- Nervous Necrosis Virus Coat Protein Mediates Host Translation Shutoff through Nuclear Translocalization and Degradation of Polyadenylate Binding Protein.Journal of virology · 2021Article
- Foot-and-Mouth Disease Virus Inhibits RIP2 Protein Expression to Promote Viral Replication.Virologica Sinica · 2021Article
- LARP1 and LARP4: up close with PABP for mRNA 3' poly(A) protection and stabilization.RNA biology · 2021Review
- DHAV-1 Blocks the Signaling Pathway Upstream of Type I Interferon by Inhibiting the Interferon Regulatory Factor 7 Protein.Frontiers in microbiology · 2021Article
- Duck Hepatitis A Virus Type 1 Induces eIF2α Phosphorylation-Dependent Cellular Translation ShutoffFrontiers in microbiology · 2021Article
- The role of host eIF2α in viral infection.Virology journal · 2020Review
- Seneca Valley Virus 3CPathogens (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During viral infections, some viruses subvert the host proteins to promote the translation or RNA replication with their protease-mediated cleavage. Poly (A)-binding protein (PABP) is a target for several RNA viruses; however, the impact of duck hepatitis A virus (DHAV) on PABP remains unknown. In this study, we demonstrated for the first time that DHAV infection stimulates a decrease in endogenous PABP and generates two cleavage fragments. On the basis of in vitro cleavage assays, an accumulation of PABP cleavage fragments was detected in duck embryo fibroblast (DEF) cell extracts incubated with functional DHAV 3C protease. In addition, DHAV 3C protease was sufficient for the cleavage of recombinant PABP without the assistance of other eukaryotic cellular cofactors. Furthermore, using site-directed mutagenesis, our data demonstrated a 3C protease cleavage site located between Q367 and G368 in duck PABP. Moreover, the knockdown of PABP inhibited the production of viral RNA, and the C-terminal domain of PABP caused a reduction in viral replication compared to the N-terminal domain. Taken together, these findings suggested that DHAV 3C protease mediates the cleavage of PABP, which may be a strategy to manipulate viral replication.
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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.