ArticleThe Journal of infectious diseases2011
Contribution of Sec61α to the life cycle of Ebola virus.
Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- A comprehensive SARS-CoV-2-human protein-protein interactome network identifies pathobiology and host-targeting therapies for COVID-19.Research square · 2022Article
- Ebola virus VP35 hijacks the PKA-CREB1 pathway for replication and pathogenesis by AKIP1 association.Nature communications · 2022Article
- Unconventional RNA-binding proteins step into the virus-host battlefront.Wiley interdisciplinary reviews. RNA · 2018Review
- Article
- A genome-wide siRNA screen identifies a druggable host pathway essential for the Ebola virus life cycle.Genome medicine · 2018Article
- Targeting Viral Proteostasis Limits Influenza Virus, HIV, and Dengue Virus Infection.Immunity · 2016Article
- Crystal structure of Marburg virus VP24.Journal of virology · 2014Article
- DNA topoisomerase 1 facilitates the transcription and replication of the Ebola virus genome.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSimilar to other viruses, the viral proteins of Ebola virus (EBOV) interact with a variety of host proteins for its replication. Of the 7 structural proteins encoded in the EBOV genome, VP24 is the smallest and is multifunctional.
methodsTo identify host factors that interact with VP24 and are required for EBOV replication, we transfected 293 cells with plasmid expressing FLAG- and HA-tagged VP24, immunoprecipitated the host proteins that bound to VP24, and analyzed the immunoprecipitants with use of mass spectrometry.
resultsOf the 68 candidate host proteins identified, we selected Sec61α because of its similar intracellular localization to that of VP24 (ie, perinuclear region), its involvement in various biological functions, and its roles in pathogenesis, such as type 2 diabetes and hepatosteatosis, and investigated its possible role in the EBOV life cycle. Our results suggest that Sec61α is not involved in EBOV entry, interferon antagonism by VP24, nucleocapsid formation, or budding. However, Sec61α colocalized with VP24 contributed to the ability of VP24 to inhibit EBOV genome transcription and reduced the polymerase activity of EBOV.
conclusionsThe present study indicates that Sec61α is a host protein involved in EBOV replication, specifically in EBOV genome transcription and replication.
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