ArticleJournal of virology2010
Role of N-linked glycosylation of the 5-HT2A receptor in JC virus infection.
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 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
- Progressive Multifocal Leukoencephalopathy Initially Considered as Central Nervous System Involvement of Post-Transplant Lymphoproliferative Disorder: The Critical Role of Contrast Enhancement on Magnetic Resonance Imaging.Internal medicine (Tokyo, Japan) · 2026Article
- Neurovascular pericytes are susceptible to infection by JC polyomavirus.Journal of virology · 2025Article
- Is dolichol pathway dysfunction a significant factor in Alzheimer's disease?Inflammopharmacology · 2025Review
- Article
- High-throughput drug screen identifies calcium and calmodulin inhibitors that reduce JCPyV infection.Antiviral research · 2024Article
- A Blood Test for the Diagnosis of Multiple Sclerosis.International journal of molecular sciences · 2024Article
- Polyomavirus Wakes Up and Chooses Neurovirulence.Viruses · 2023Review
- Dynamics and Patterning of 5-Hydroxytryptamine 2 Subtype Receptors in JC Polyomavirus Entry.Viruses · 2022Article
- Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection.Viruses · 2022Review
- The oncogenic roles of JC polyomavirus in cancer.Frontiers in oncology · 2022Review
- GRK2 mediates β-arrestin interactions with 5-HTJournal of virology · 2021Article
- International Union of Basic and Clinical Pharmacology. CX. Classification of Receptors for 5-hydroxytryptamine; Pharmacology and Function.Pharmacological reviews · 2021Review
- Review
- Adipocyte Plasma Membrane Protein (APMAP) promotes JC Virus (JCPyV) infection in human glial cells.Virology · 2020Article
- Glycoproteome in silkworm Bombyx mori and alteration by BmCPV infection.Journal of proteomics · 2020Article
- Evidence of the Mechanism by Which Polyomaviruses Exploit the Extracellular Vesicle Delivery System during Infection.Viruses · 2020Review
- Host receptors: the key to establishing cells with broad viral tropism for vaccine production.Critical reviews in microbiology · 2020Review
- Microtubules in Polyomavirus Infection.Viruses · 2020Review
- Host-Immune Interactions in JC Virus Reactivation and Development of Progressive Multifocal Leukoencephalopathy (PML).Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- Heparan Sulfate Proteoglycans and Viral Attachment: True Receptors or Adaptation Bias?Viruses · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
JC virus (JCV) is a human polyomavirus and the causative agent of the fatal demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV infection of host cells is dependent on interactions with cell surface asparagine (N)-linked sialic acids and the serotonin 5-hydroxytryptamine(2A) receptor (5-HT(2A)R). The 5-HT(2A)R contains five potential N-linked glycosylation sites on the extracellular N terminus. Glycosylation of other serotonin receptors is essential for expression, ligand binding, and receptor function. Also, glycosylation of cellular receptors has been reported to be important for JCV infection. Therefore, we hypothesized that the 5-HT(2A)R N-linked glycosylation sites are required for JCV infection. Treatment of 5-HT(2A)R-expressing cells with tunicamycin, an inhibitor of N-linked glycosylation, reduced JCV infection. Individual mutation of each of the five N-linked glycosylation sites did not affect the capacity of 5-HT(2A)R to support JCV infection and did not alter the cell surface expression of the receptor. However, mutation of all five N-linked glycosylation sites simultaneously reduced the capacity of 5-HT(2A)R to support infection and altered the cell surface expression. Similarly, tunicamycin treatment reduced the cell surface expression of 5-HT(2A)R. Mutation of all five N-linked glycosylation sites or tunicamycin treatment of cells expressing wild-type 5-HT(2A)R resulted in an altered electrophoretic mobility profile of the receptor. Treatment of cells with PNGase F, to remove N-linked oligosaccharides from the cell surface, did not affect JCV infection in 5-HT(2A)R-expressing cells. These data affirm the importance of 5-HT(2A)R as a JCV receptor and demonstrate that the sialic acid component of the receptor is not directly linked to 5-HT(2A)R.
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Registered trials
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