ArticleVirus genes2010
Functional analysis of Spodoptera litura nucleopolyhedrovirus p49 gene during Autographa californica nucleopolyhedrovirus infection of SpLi-221 cells.
Article in Virus genes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 14 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
- Generating a host range-expanded recombinant baculovirus.Scientific reports · 2016Article
- The Baculovirus Antiapoptotic p35 Protein Functions as an Inhibitor of the Host RNA Interference Antiviral Response.Journal of virology · 2015Article
- Novel apoptosis suppressor Apsup from the baculovirus Lymantria dispar multiple nucleopolyhedrovirus precludes apoptosis by preventing proteolytic processing of initiator caspase Dronc.Journal of virology · 2013Article
- Baculovirus infection induces a DNA damage response that is required for efficient viral replication.Journal of virology · 2011Article
Corrections and comments
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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
The Spodoptera litura nucleopolyhedrovirus (SpltNPV) antiapoptotic gene Splt-p49 is able to rescue replication of a p35-null Autographa californica nucleopolyhedrovirus (AcMNPV) in AcMNPV-permissive Sf9 cells. In this study, an AcMNPV p35 knockout bacmid was generated through ET homologous recombination in Escherichia coli and designated as vAc(P35-KO). The Splt-p49 gene was transposed into the polyhedrin locus of vAc(P35-KO) to investigate if Splt-p49 has any antiapoptotic activity in the context of AcMNPV infection of AcMNPV-nonpermissive SpLi-221 cells. Our results demonstrated that Splt-p49 could not inhibit the apoptosis induced by AcMNPV infection of SpLi-221 cells when it was under the control of its native promoter. Western blot analysis showed that Splt-P49 was poorly expressed. When the expression of Splt-P49 was under the control of Drosophila hsp70 promoter, the expression of Splt-P49 was advanced, and a higher level of Splt-P49 was detected. As a result, the apoptosis of SpLi-221 cells was inhibited; however, budded-virus production did not improve in comparison with that in AcMNPV-infected SpLi-221 cells. These data indicated that there are other barrier(s) to AcMNPV replication in the nonpermissive SpLi-221 cells besides apoptosis.
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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.