Evidence map›Paper›PMID 35475666›Full record

ArticleJournal of virology2022

Role of the Orphan Transporter SLC35E1 in the Nuclear Egress of Herpes Simplex Virus 1.

Fumio Maeda, Akihisa Kato, Kosuke Takeshima, Misato Shibazaki, Ryota Sato, Takuma Shibata, Kensuke Miyake, Hiroko Kozuka-Hata, Masaaki Oyama, Eigo Shimizu and 9 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Fumio MaedaDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Akihisa KatoDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Kosuke TakeshimaDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Misato ShibazakiDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Ryota SatoDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Takuma ShibataDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Kensuke MiyakeDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Hiroko Kozuka-HataMedical Proteomics Laboratory, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Masaaki OyamaMedical Proteomics Laboratory, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Eigo ShimizuLaboratory DNA Information Analysis, Human Genome Center, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Seiya ImotoLaboratory Health Medical Intelligence, Human Genome Center, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Satoru MiyanoLaboratory DNA Information Analysis, Human Genome Center, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Shungo AdachiCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tokyo, Japan.
Tohru NatsumeCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tokyo, Japan.
Koh TakeuchiCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tokyo, Japan.
Yuhei MaruzuruDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Naoto KoyanagiDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Arii JunDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.
Kawaguchi YasushiDivision of Molecular Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyogrid.26999.3d, Tokyo, Japan.ORCID 0000-0001-8232-6925
National Institute of Infectious Diseases · JPThe University of Tokyo · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study developed a system consisting of two rounds of screening cellular proteins involved in the nuclear egress of herpes simplex virus 1 (HSV-1). Using this system, we first screened cellular proteins that interacted with the HSV-1 nuclear egress complex (NEC) consisting of UL34 and UL31 in HSV-1-infected cells, which are critical for the nuclear egress of HSV-1, by tandem affinity purification coupled with mass spectrometry-based proteomics technology. Next, we performed CRISPR/Cas9-based screening of live HSV-1-infected reporter cells under fluorescence microscopy using single guide RNAs targeting the cellular proteins identified in the first proteomic screening to detect the mislocalization of the lamin-associated protein emerin, which is a phenotype for defects in HSV-1 nuclear egress. This study focused on a cellular orphan transporter SLC35E1, one of the cellular proteins identified by the screening system. Knockout of SLC35E1 reduced HSV-1 replication and induced membranous invaginations containing perinuclear enveloped virions (PEVs) adjacent to the nuclear membrane (NM), aberrant accumulation of PEVs in the perinuclear space between the inner and outer NMs and the invagination structures, and mislocalization of the NEC. These effects were similar to those of previously reported mutation(s) in HSV-1 proteins and depletion of cellular proteins that are important for HSV-1 de-envelopment, one of the steps required for HSV-1 nuclear egress. Our newly established screening system enabled us to identify a novel cellular protein required for efficient HSV-1 de-envelopment.

Indexed as

Herpesvirus 1, HumanMembrane Transport ProteinsVirus ReleaseAnimalsChlorocebus aethiopsCRISPR-Cas SystemsGene Knockout TechniquesHEK293 CellsHeLa CellsHumansNuclear EnvelopeNuclear ProteinsProteomicsVero CellsViral ProteinsMembrane Transport ProteinsNuclear ProteinsUL31 protein, Human herpesvirus 1UL34 protein, Human herpesvirus 1Viral ProteinsHSV-1nuclear egressSLC35E1transporter

Identifiers

PMID35475666
PMCPMC9131867
OpenAlexW4224985745

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.