ArticleProceedings of the National Academy of Sciences of the United States of America2018
HIV-1 gag recruits PACSIN2 to promote virus spreading.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Incorporation of genome-bound cellular proteins into HIV-1 particles regulates viral infection.Cell reports · 2026Article
- The ectodomain sheddase ADAM10 restricts HIV-1 propagation and is counteracted by Nef.Science advances · 2025Article
- Identification of the role of SNARE proteins in rAAV vector production through interaction with the viral MAAP.Molecular therapy. Methods & clinical development · 2025Article
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- PACSIN proteins in vivo: Roles in development and physiology.Acta physiologica (Oxford, England) · 2022Review
- HIV-1 propagation is highly dependent on basal levels of the restriction factor BST2.Science advances · 2021Article
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- A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis.Nature communications · 2021Article
- Key interplay between the co-opted sorting nexin-BAR proteins and PI3P phosphoinositide in the formation of the tombusvirus replicase.PLoS pathogens · 2020Article
- How HIV-1 Gag Manipulates Its Host Cell Proteins: A Focus on Interactors of the Nucleocapsid Domain.Viruses · 2020Review
- PACSIN2 Interacts with Nonstructural Protein 5A and Regulates Hepatitis C Virus Assembly.Journal of virology · 2020Article
- From Entry to Egress: Strategic Exploitation of the Cellular Processes by HIV-1.Frontiers in microbiology · 2020Review
- NEDD4 family ubiquitin ligases associate with LCMV Z's PPXY domain and are required for virus budding, but not via direct ubiquitination of Z.PLoS pathogens · 2019Article
- Article
- HIV-1 packs in PACSIN2 for cell-to-cell spread.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The p2b domain of Rous sarcoma virus (RSV) Gag and the p6 domain of HIV-1 Gag contain late assembly (L) domains that engage the ESCRT membrane fission machinery and are essential for virus release. We now show that the PPXY-type RSV L domain specifically recruits the BAR domain protein PACSIN2 into virus-like particles (VLP), in addition to the NEDD4-like ubiquitin ligase ITCH and ESCRT pathway components such as TSG101. PACSIN2, which has been implicated in the remodeling of cellular membranes and the actin cytoskeleton, is also recruited by HIV-1 p6 independent of its ability to engage the ESCRT factors TSG101 or ALIX. Moreover, PACSIN2 is robustly recruited by NEDD4-2s, a NEDD4-like ubiquitin ligase capable of rescuing HIV-1 budding defects. The NEDD4-2s-induced incorporation of PACSIN2 into VLP correlated with the formation of Gag-ubiquitin conjugates, indicating that PACSIN2 binds ubiquitin. Although PACSIN2 was not required for a single cycle of HIV-1 replication after infection with cell-free virus, HIV-1 spreading was nevertheless severely impaired in T cell lines and primary human peripheral blood mononuclear cells depleted of PACSIN2. HIV-1 spreading could be restored by reintroduction of wild-type PACSIN2, but not of a SH3 domain mutant unable to interact with the actin polymerization regulators WASP and N-WASP. Overall, our observations indicate that PACSIN2 promotes the cell-to-cell spreading of HIV-1 by connecting Gag to the actin cytoskeleton.
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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 Socratic graph.