ArticleScientific reports2013
Adaptor protein complexes-1 and 3 are involved at distinct stages of flavivirus life-cycle.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Development of pyrazolo[1,5-a]pyrimidine based macrocyclic kinase inhibitors targeting AAK1.European journal of medicinal chemistry · 2025Article
- Adaptor protein complex 1 gamma 1 subunit is an important host factor involved in both Zika virus and dengue virus infections.Virologica Sinica · 2025Article
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
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- Host proteins interact with viral elements and affect the life cycle of highly pathogenic avian influenza A virus H7N9.Heliyon · 2024Article
- Dengue virus replication enhances labile zinc pools by modulation of ZIP8.Cellular microbiology · 2021Article
- Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species.International journal of molecular sciences · 2021Review
- TRANSPIRE: A Computational Pipeline to Elucidate Intracellular Protein Movements from Spatial Proteomics Data Sets.Journal of the American Society for Mass Spectrometry · 2020Article
- Suppression of µ1 subunit of the adaptor protein complex 2 reduces dengue virus release.Virus genes · 2020Article
- Isolation and molecular characterization of dengue virus clinical isolates from pediatric patients in New Delhi.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2019Article
- Zinc Chelation Specifically Inhibits Early Stages of Dengue Virus Replication by Activation of NF-κB and Induction of Antiviral Response in Epithelial Cells.Frontiers in immunology · 2019Article
- Viral journeys on the intracellular highways.Cellular and molecular life sciences : CMLS · 2018Review
- Article
- Anticancer kinase inhibitors impair intracellular viral trafficking and exert broad-spectrum antiviral effects.The Journal of clinical investigation · 2017Article
- CD8 T cells protect adult naive mice from JEV-induced morbidity via lytic function.PLoS neglected tropical diseases · 2017Article
- Platelet activation determines the severity of thrombocytopenia in dengue infection.Scientific reports · 2017Article
- Dengue Virus Entry and Replication Does Not Lead to Productive Infection in Platelets.Open forum infectious diseases · 2017Article
- Dengue Virus Capsid Interacts with DDX3X-A Potential Mechanism for Suppression of Antiviral Functions in Dengue Infection.Frontiers in cellular and infection microbiology · 2017Article
- N-Desmethylclozapine, Fluoxetine, and Salmeterol Inhibit Postentry Stages of the Dengue Virus Life Cycle.Antimicrobial agents and chemotherapy · 2016Article
- Identification and characterization of the role of c-terminal Src kinase in dengue virus replication.Scientific reports · 2016Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular protein trafficking pathways are hijacked by viruses at various stages of viral life-cycle. Heterotetrameric adaptor protein complexes (APs) mediate vesicular trafficking at distinct intracellular sites and are essential for maintaining the organellar homeostasis. In the present study, we studied the effect of AP-1 and AP-3 deficiency on flavivirus infection in cells functionally lacking these proteins. We show that AP-1 and AP-3 participate in flavivirus life-cycle at distinct stages. AP-3-deficient cells showed delay in initiation of Japanese encephalitis virus and dengue virus RNA replication, which resulted in reduction of infectious virus production. AP-3 was found to colocalize with RNA replication compartments in infected wild-type cells. AP-1 deficiency affected later stages of dengue virus infection where increased intracellular accumulation of infectious virus was observed. Therefore, our results propose a novel role for AP-1 and AP-3 at distinct stages of infection of some of the RNA viruses.
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