ArticleBiochemical and biophysical research communications2014
TGEV nucleocapsid protein induces cell cycle arrest and apoptosis through activation of p53 signaling.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Characterization of nucleolar localization signals in the avian infectious bronchitis virus nucleocapsid protein and their critical role in viral replication.Journal of virology · 2026Article
- Rapid and visual detection of transmissible gastroenteritis virus using a CRISPR/Cas12a system combined with loop-mediated isothermal amplification.BMC veterinary research · 2025Article
- Coronavirus nucleocapsid proteins: a multifaceted modulator in the innate immune evasion.Frontiers in microbiology · 2025Review
- Mechanism by which porcine transmissible gastroenteritis virus disrupts host innate immunity.Frontiers in immunology · 2025Review
- Coronavirus nucleocapsid protein enhances the binding of p-PKCα to RACK1: Implications for inhibition of nucleocytoplasmic trafficking and suppression of the innate immune response.PLoS pathogens · 2024Article
- Coronavirus RNA-dependent RNA polymerase interacts with the p50 regulatory subunit of host DNA polymerase delta and plays a synergistic role with RNA helicase in the induction of DNA damage response and cell cycle arrest in the S phase.Emerging microbes & infections · 2023Article
- Roles of p53-Mediated Host-Virus Interaction in Coronavirus Infection.International journal of molecular sciences · 2023Review
- Review
- Porcine Circovirus 2 Activates the PERK-Reactive Oxygen Species Axis To Induce p53 Phosphorylation with Subsequent Cell Cycle Arrest at S Phase in Favor of Its Replication.Journal of virology · 2022Article
- Up-regulated 60S ribosomal protein L18 in PEDV N protein-induced S-phase arrested host cells promotes viral replication.Virus research · 2022Article
- The Effects of Swine Coronaviruses on ER Stress, Autophagy, Apoptosis, and Alterations in Cell Morphology.Pathogens (Basel, Switzerland) · 2022Review
- Swine Enteric Coronavirus: Diverse Pathogen-Host Interactions.International journal of molecular sciences · 2022Review
- All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Apoptosis in IPEC-J2 Cells via Inhibiting ROS-Mediated PAntioxidants (Basel, Switzerland) · 2022Article
- Interplay between swine enteric coronaviruses and host innate immune.Frontiers in veterinary science · 2022Review
- Modulation of Innate Antiviral Immune Response by Porcine Enteric Coronavirus.Frontiers in microbiology · 2022Review
- Coronavirus Porcine Epidemic Diarrhea Virus Nucleocapsid Protein Interacts with p53 To Induce Cell Cycle Arrest in S-Phase and Promotes Viral Replication.Journal of virology · 2021Article
- Recent Progress in Torovirus Molecular Biology.Viruses · 2021Review
- Animal Coronaviruses Induced Apoptosis.Life (Basel, Switzerland) · 2021Review
- Characterization of Localization and Export Signals of Bovine Torovirus Nucleocapsid Protein Responsible for Extensive Nuclear and Nucleolar Accumulation and Their Importance for Virus Growth.Journal of virology · 2021Article
- PRRSV Promotes MARC-145 Cells Entry Into S Phase of the Cell Cycle to Facilitate Viral ReplicationFrontiers in veterinary science · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous studies showed that TGEV infection could induce cell cycle arrest and apoptosis via activation of p53 signaling in cultured host cells. However, it is unclear which viral gene causes these effects. In this study, we investigated the effects of TGEV nucleocapsid (N) protein on PK-15 cells. We found that TGEV N protein suppressed cell proliferation by causing cell cycle arrest at the S and G2/M phases and apoptosis. Characterization of various cellular proteins that are involved in regulating cell cycle progression demonstrated that the expression of N gene resulted in an accumulation of p53 and p21, which suppressed cyclin B1, cdc2 and cdk2 expression. Moreover, the expression of TGEV N gene promoted translocation of Bax to mitochondria, which in turn caused the release of cytochrome c, followed by activation of caspase-3, resulting in cell apoptosis in the transfected PK-15 cells following cell cycle arrest. Further studies showed that p53 inhibitor attenuated TGEV N protein induced cell cycle arrest at S and G2/M phases and apoptosis through reversing the expression changes of cdc2, cdk2 and cyclin B1 and the translocation changes of Bax and cytochrome c induced by TGEV N protein. Taken together, these results demonstrated that TGEV N protein might play an important role in TGEV infection-induced p53 activation and cell cycle arrest at the S and G2/M phases and apoptosis occurrence.
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