ArticleJournal of virology2000
Directional transneuronal infection by pseudorabies virus is dependent on an acidic internalization motif in the Us9 cytoplasmic tail.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 68 citations in OpenAlex.
- The US9-Derived Protein gPTB9TM Modulates APP Processing Without Targeting Secretase Activities.Molecular neurobiology · 2023Article
- Use of a tissue clearing technique combined with retrograde trans-synaptic viral tracing to evaluate changes in mouse retinorecipient brain regions following optic nerve crush.Neural regeneration research · 2023Article
- Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses.Viruses · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- Pseudorabies Virus Infection Accelerates Degradation of the Kinesin-3 Motor KIF1A.Journal of virology · 2020Article
- Microtubule-Dependent Trafficking of Alphaherpesviruses in the Nervous System: The Ins and Outs.Viruses · 2019Review
- Kinesin-1 Proteins KIF5A, -5B, and -5C Promote Anterograde Transport of Herpes Simplex Virus Enveloped Virions in Axons.Journal of virology · 2018Article
- The lipid raft-dwelling protein US9 can be manipulated to target APP compartmentalization, APP processing, and neurodegenerative disease pathogenesis.Scientific reports · 2017Article
- Molecular association of herpes simplex virus type 1 glycoprotein E with membrane protein Us9.Archives of virology · 2016Article
- The Basic Domain of Herpes Simplex Virus 1 pUS9 Recruits Kinesin-1 To Facilitate Egress from Neurons.Journal of virology · 2016Article
- Genome Sequence of the Anterograde-Spread-Defective Herpes Simplex Virus 1 Strain MacIntyre.Genome announcements · 2014Article
- Herpes simplex virus gE/gI extracellular domains promote axonal transport and spread from neurons to epithelial cells.Journal of virology · 2014Article
- Long-term Cre-mediated retrograde tagging of neurons using a novel recombinant pseudorabies virus.Frontiers in neuroanatomy · 2014Article
- Article
- Delivery of herpes simplex virus to retinal ganglion cell axon is dependent on viral protein Us9.Investigative ophthalmology & visual science · 2013Article
- Herpes simplex virus membrane proteins gE/gI and US9 act cooperatively to promote transport of capsids and glycoproteins from neuron cell bodies into initial axon segments.Journal of virology · 2013Article
- Role of Us9 phosphorylation in axonal sorting and anterograde transport of pseudorabies virus.PloS one · 2013Article
- Kinesin-3 mediates axonal sorting and directional transport of alphaherpesvirus particles in neurons.Cell host & microbe · 2012Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Us9 gene is conserved among most alphaherpesviruses. In pseudorabies virus (PRV), the Us9 protein is a 98-amino-acid, type II membrane protein found in the virion envelope. It localizes to the trans-Golgi network (TGN) region in infected and transfected cells and is maintained in this compartment by endocytosis from the plasma membrane. Viruses with Us9 deleted have no observable defects in tissue culture yet have reduced virulence and restricted spread to retinorecipient neurons in the rodent brain. In this report, we demonstrate that Us9-promoted transneuronal spread in vivo is dependent on a conserved acidic motif previously shown to be essential for the maintenance of Us9 in the TGN region and recycling from the plasma membrane. Mutant viruses with the acidic motif deleted have an anterograde spread defect indistinguishable from that of Us9 null viruses. Transneuronal spread, however, is not dependent on a dileucine endocytosis motif in the Us9 cytoplasmic tail. Through alanine scanning mutagenesis of the acidic motif, we have identified two conserved tyrosine residues that are essential for Us9-mediated spread as well as two serine residues, comprising putative consensus casein kinase II sites, that modulate the rate of PRV transneuronal spread in vivo.
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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.