ArticleJournal of virology2007
The YLDL sequence within Sendai virus M protein is critical for budding of virus-like particles and interacts with Alix/AIP1 independently of C protein.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
- Nonlytic Egress and Transmission in the Virus World.Annual review of biochemistry · 2025Review
- Insights into the function of ESCRT and its role in enveloped virus infection.Frontiers in microbiology · 2023Review
- Nonlytic cellular release of hepatitis A virus requires dual capsid recruitment of the ESCRT-associated Bro1 domain proteins HD-PTP and ALIX.PLoS pathogens · 2022Article
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- Structural Insight into the Interaction of Sendai Virus C Protein with Alix To Stimulate Viral Budding.Journal of virology · 2021Article
- The Integrity of the YxxL Motif of Ebola Virus VP24 Is Important for the Transport of Nucleocapsid-Like Structures and for the Regulation of Viral RNA Synthesis.Journal of virology · 2020Article
- Genomic characterization, phylogenetic position and in situ localization of a novel putative mononegavirus in Lepeophtheirus salmonis.Archives of virology · 2019Article
- Structural analysis of the STAT1:STAT2 heterodimer revealed the mechanism of Sendai virus C protein-mediated blockade of type 1 interferon signaling.The Journal of biological chemistry · 2017Article
- Loss of Sendai virus C protein leads to accumulation of RIG-I immunostimulatory defective interfering RNA.The Journal of general virology · 2017Article
- Nipah virus matrix protein: expert hacker of cellular machines.FEBS letters · 2016Review
- ESCRT Requirements for Murine Leukemia Virus Release.Viruses · 2016Article
- Analysis of Assembly and Budding of Lujo Virus.Journal of virology · 2015Article
- ALIX Rescues Budding of a Double PTAP/PPEY L-Domain Deletion Mutant of Ebola VP40: A Role for ALIX in Ebola Virus Egress.The Journal of infectious diseases · 2015Article
- Evidence for ubiquitin-regulated nuclear and subnuclear trafficking among Paramyxovirinae matrix proteins.PLoS pathogens · 2015Article
- A leucine residue in the C terminus of human parainfluenza virus type 3 matrix protein is essential for efficient virus-like particle and virion release.Journal of virology · 2014Article
- Galectin-3 promotes HIV-1 budding via association with Alix and Gag p6.Glycobiology · 2014Article
- Sendai virus C proteins regulate viral genome and antigenome synthesis to dictate the negative genome polarity.Journal of virology · 2014Article
- Review
- Alix serves as an adaptor that allows human parainfluenza virus type 1 to interact with the host cell ESCRT system.PloS one · 2013Article
- Functional characterization of the putative hepatitis B virus core protein late domain using retrovirus chimeras.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For many enveloped viruses, cellular multivesicular body (MVB) sorting machinery has been reported to be utilized for efficient viral budding. Matrix and Gag proteins have been shown to contain one or two L-domain motifs (PPxY, PT/SAP, YPDL, and FPIV), some of which interact specifically with host cellular proteins involved in MVB sorting, which are recruited to the viral budding site. However, for many enveloped viruses, L-domain motifs have not yet been identified and the involvement of MVB sorting machinery in viral budding is still unknown. Here we show that both Sendai virus (SeV) matrix protein M and accessory protein C contribute to virus budding by physically interacting with Alix/AIP1. A YLDL sequence within the M protein showed L-domain activity, and its specific interaction with the N terminus of Alix/AIP1(1-211) was important for the budding of virus-like particles (VLPs) of M protein. In addition, M-VLP budding was inhibited by the overexpression of some deletion mutant forms of Alix/AIP1 and depletion of endogenous Alix/AIP1 with specific small interfering RNAs. The YLDL sequence was not replaceable by other L-domain motifs, such as PPxY and PT/SAP, and even YPxL. C protein was also able to physically interact with the N terminus of Alix/AIP1(212-357) and enhanced M-VLP budding independently of M-Alix/AIP1 interaction, although it was not released from the transfected cells itself. Our results suggest that the interaction of multiple viral proteins with Alix/AIP1 may enhance the efficiency of the utilization of cellular MVB sorting machinery for efficient SeV budding.
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