ArticleJournal of virology2010
The major determinant for addition of tegument protein pUL48 (VP16) to capsids in herpes simplex virus type 1 is the presence of the major tegument protein pUL36 (VP1/2).
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Article
- The loss of both pUL16 and pUL21 in HSV-1-infected cells alters capsid-tegument composition, nuclear membrane architecture, cytoplasmic maturation and cell-to-cell spread.The Journal of general virology · 2025Article
- The loss of both pUL16 and pUL21 in HSV-1 infected cells abolishes cytoplasmic envelopment.bioRxiv : the preprint server for biology · 2024Article
- The incredible bulk: Human cytomegalovirus tegument architectures uncovered by AI-empowered cryo-EM.Science advances · 2024Article
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
- Large Subunit of the Human Herpes Simplex Virus Terminase as a Promising Target in Design of Anti-Herpesvirus Agents.Molecules (Basel, Switzerland) · 2023Article
- Identification and classification of papain-like cysteine proteinases.The Journal of biological chemistry · 2023Article
- Review
- The herpes simplex virus tegument protein pUL21 is required for viral genome retention within capsids.PLoS pathogens · 2022Article
- Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses.Viruses · 2021Review
- A putative WAVE regulatory complex (WRC) interacting receptor sequence (WIRS) in the cytoplasmic tail of HSV-1 gE does not function in WRC recruitment or neuronal transport.Access microbiology · 2021Article
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- The ESCRT-II Subunit EAP20/VPS25 and the Bro1 Domain Proteins HD-PTP and BROX Are Individually Dispensable for Herpes Simplex Virus 1 Replication.Journal of virology · 2020Article
- The Role of VP16 in the Life Cycle of Alphaherpesviruses.Frontiers in microbiology · 2020Review
- Microtubule-Dependent Trafficking of Alphaherpesviruses in the Nervous System: The Ins and Outs.Viruses · 2019Review
- Seeking Closure: How Do Herpesviruses Recruit the Cellular ESCRT Apparatus?Journal of virology · 2019Review
- Dissecting the Herpesvirus Architecture by Targeted Proteolysis.Journal of virology · 2018Article
- Structure of the herpes simplex virus 1 capsid with associated tegument protein complexes.Science (New York, N.Y.) · 2018Article
- Molecular Evolution of Herpes Simplex Virus 2 Complete Genomes: Comparison between Primary and Recurrent Infections.Journal of virology · 2017Article
- Assembly and Egress of an Alphaherpesvirus Clockwork.Advances in anatomy, embryology, and cell biology · 2017Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study a number of herpes simplex virus type 1 (HSV-1) proteins were screened, using a yeast-two-hybrid assay, for interaction with the tegument protein pUL48 (VP16). This approach identified interactions between pUL48 and the capsid proteins pUL19 (VP5), pUL38 (VP19C), and pUL35 (VP26). In addition, the previously identified interaction of pUL48 with the major tegument protein pUL36 (VP1/2) was confirmed. All of these interactions, except that of pUL35 and pUL48, could be confirmed using an in vitro pulldown assay. A subsequent pulldown assay with intact in vitro-assembled capsids, consisting of pUL19, pUL38, and pUL18 (VP23) with or without pUL35, showed no binding of pUL48, suggesting that the capsid/pUL48 interactions initially identified were more then likely not biologically relevant. This was confirmed by using a series of HSV-1 mutants lacking the gene encoding either pUL35, pUL36, or pUL37. For each HSV-1 mutant, analysis of purified deenveloped C capsids indicated that only in the absence of pUL36 was there a complete loss of capsid-bound pUL48, as well as pUL37. Collectively, this study shows for the first time that pUL36 is a major factor for addition of both pUL48 and pUL37, likely through a direct interaction of both with nonoverlapping sites in pUL36, to unenveloped C capsids during assembly of HSV-1.
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