Evidence map›Paper›PMID 30700607›Full record

ArticleJournal of virology2019

S-Like-Phase Cyclin-Dependent Kinases Stabilize the Epstein-Barr Virus BDLF4 Protein To Temporally Control Late Gene Transcription.

Yoshitaka Sato, Takahiro Watanabe, Chihiro Suzuki, Yuichi Abe, H M Abdullah Al Masud, Tomoki Inagaki, Masahiro Yoshida, Takeshi Suzuki, Fumi Goshima, Jun Adachi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Yoshitaka Sato *Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.ORCID 0000-0002-8541-6413
Takahiro Watanabe *Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Chihiro SuzukiDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Yuichi AbeLaboratory of Proteome Research, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
H M Abdullah Al MasudDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.ORCID 0000-0002-0953-2471
Tomoki InagakiDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Masahiro YoshidaDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Takeshi SuzukiDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Fumi GoshimaDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Jun AdachiLaboratory of Proteome Research, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Takeshi TomonagaLaboratory of Proteome Research, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Takayuki MurataDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Hiroshi KimuraDepartment of Virology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan hkimura@med.nagoya-u.ac.jp.ORCID 0000-0001-8063-5660
Nagoya University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPFujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Temporally controlled gene expression is necessary for the propagation of herpesviruses. To achieve this, herpesviruses encode several transcriptional regulators. In Epstein-Barr virus, BcRF1 associates with five viral proteins (BDLF4, BGLF3, BFRF2, BVLF1, and BDLF3.5) to form the viral late (L) gene regulatory complex, which is called the viral preinitiation complex (vPIC), on TATT-containing promoters. However, regulation of the vPIC has been largely unexplored. In this study, we performed two screens using a kinase inhibitor library and identified a series of cyclin-dependent kinase (CDK) inhibitors that downregulated the expression of L genes without any impact on viral DNA replication through destabilization of the BDLF4 protein. Knockdown of CDK2 by short hairpin RNA (shRNA) and proteasome inhibitor treatment showed that phosphorylation of the BDLF4 protein prevented ubiquitin-mediated degradation. Moreover, we demonstrated that cyclin A- and E-associated CDK2 complexes phosphorylated BDLF4

Indexed as

Gene Expression Regulation, ViralProteolysisTranscription, GeneticCyclin-Dependent Kinase 2Gene Knockdown TechniquesHEK293 CellsHerpesvirus 4, HumanHumansPhosphorylationProteasome InhibitorsProtein StabilityUbiquitinViral ProteinsCDK2 protein, humanCyclin-Dependent Kinase 2Proteasome InhibitorsUbiquitinViral ProteinsBDLF4CDK2EBVphosphorylationvPIC

Identifiers

PMID30700607
PMCPMC6450117
OpenAlexW2912210717

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.