ArticleVirus research2010
Influenza virus budding does not require a functional AAA+ ATPase, VPS4.
Article in Virus research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Influenza A virus RNA localisation and the interceding trafficking pathways of the host cell.PLoS pathogens · 2025Review
- Structural Insight into the Interaction of Sendai Virus C Protein with Alix To Stimulate Viral Budding.Journal of virology · 2021Article
- Role of Extracellular Vesicles in Influenza Virus Infection.Frontiers in cellular and infection microbiology · 2020Review
- Effects of Inhibiting VPS4 Support a General Role for ESCRTs in Extracellular Vesicle Biogenesis.Biophysical journal · 2017Article
- Up-regulation of Vps4A promotes neuronal apoptosis after intracerebral hemorrhage in adult rats.Metabolic brain disease · 2017Article
- High CHMP4B expression is associated with accelerated cell proliferation and resistance to doxorubicin in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- [Analysis of differentially expressed proteome in urine from non-small cell lung cancer patients].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015Article
- In vitro evolution of high-titer, virus-like vesicles containing a single structural protein.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Compounds with anti-influenza activity: present and future of strategies for the optimal treatment and management of influenza. Part I: Influenza life-cycle and currently available drugs.Journal of preventive medicine and hygiene · 2014Review
- Type I interferon imposes a TSG101/ISG15 checkpoint at the Golgi for glycoprotein trafficking during influenza virus infection.Cell host & microbe · 2013Article
- Vacuolar protein sorting 4B, an ATPase protein positively regulates the progression of NSCLC via promoting cell division.Molecular and cellular biochemistry · 2013Article
- How to get out: ssRNA enveloped viruses and membrane fission.Current opinion in virology · 2013Review
- Viral membrane scission.Annual review of cell and developmental biology · 2013Review
- F1Fo-ATPase, F-type proton-translocating ATPase, at the plasma membrane is critical for efficient influenza virus budding.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Cellular VPS4 is required for efficient entry and egress of budded virions of Autographa californica multiple nucleopolyhedrovirus.Journal of virology · 2012Article
- Human immunodeficiency virus rev-binding protein is essential for influenza a virus replication and promotes genome trafficking in late-stage infection.Journal of virology · 2011Article
- Influenza virus is not restricted by tetherin whereas influenza VLP production is restricted by tetherin.Virology · 2011Article
- A Rab11- and microtubule-dependent mechanism for cytoplasmic transport of influenza A virus viral RNA.Journal of virology · 2011Article
- Influenza virus assembly and budding.Virology · 2011Review
- Un-“ESCRT”-ed budding.Viruses · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The process of budding of many enveloped viruses utilizes the cellular ESCRT (endosomal sorting complex required for transport) machinery, that is normally involved in the formation of luminal vesicles of endosomal multivesiculate bodies (MVB). A late step in the MVB pathway involves the recruitment of VPS4, an AAA+ ATPase, to the ESCRT complexes. Our earlier work had shown that the formation of influenza virus-like particles was not inhibited by dominant negative VPS4A. However, it was not known if there was a role of VPS4 and the ESCRT pathway in influenza virus particle budding and this needed to be investigated. It was found that neither siRNA knockdown of VPS4A and VPS4B expression nor the use of cell lines that inducibly express VPS4A or VPS4B dominant negative mutants, inhibited influenza virus budding. In contrast, and in keeping with more recent data, vesicular stomatitis virus budding was diminished by VPS4 dysfunction.
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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.