ArticleMolecular and cellular biochemistry2016
Baculovirus antiapoptotic protein P35 regulated the host apoptosis to enhance virus multiplication.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 15 citations in OpenAlex.
- The Expression of P35 Plays a Key Role in the Difference in Apoptosis Induced by AcMNPV Infection in DifferentInternational journal of molecular sciences · 2023Article
- Ac154 carried out anti-apoptotic role during AcMNPV infection process in the host insect cells.Molecular and cellular biochemistry · 2020Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) possesses p35 gene, which encodes antiapoptosis protein P35 (or Ac-P35). A previous study showed that deleting p35 promoted premature cytolysis and caused the reduction of virus yield. In this report, we examined the role of P35 in regulating the expression of Ac-IAPs (inhibitor of apoptosis proteins in AcMNPV) and SfP53 (an apoptosis protein in Sf9 cells), and its effect on the production of progeny virus. Results showed that the overexpression of P35 caused a delay in the increase process of SfP53 before 36-h post infection and improved the transcription levels of iaps gene dramatically; it was more favorable to improve the transcription level of iap1 at 24-72 h post infection. Moreover, P35 could promote the production of progeny virus. This is the first study to disclose the relationship among p35, iap1, iap2, Sfp53 and the replication of the virus in the AcMNPV infection process, which provides the basis for improving the insecticidal activity of recombinant AcMNPV in terms of theory and technology.
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