Evidence map›Paper›PMID 29167347›Full record

ArticleJournal of virology2018

Novel Role of vBcl2 in the Virion Assembly of Kaposi's Sarcoma-Associated Herpesvirus.

Qiming Liang, Dahai Wei, Brian Chung, Kevin F Brulois, Changrun Guo, Shupeng Dong, Shou-Jiang Gao, Pinghui Feng, Chengyu Liang, Jae U Jung

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Review
  7. Human Gammaherpesvirus 8 Oncogenes Associated with Kaposi's Sarcoma.International journal of molecular sciences · 2022
    Review
  8. Article
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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

10 authors at 2 institutions in 2 countries.

Qiming Liang *Shanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China liangqiming@shsmu.edu.cn jaeujung@med.usc.edu.
Dahai Wei *Shanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Brian ChungDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Kevin F BruloisDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Changrun GuoShanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shupeng DongShanghai Institute of Immunology, Department of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shou-Jiang GaoDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Pinghui FengDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Chengyu LiangDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.
Jae U JungDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA liangqiming@shsmu.edu.cn jaeujung@med.usc.edu.
University of Southern California · USShanghai Jiao Tong University · CN

Funding

Cell Model for KSHV Infection and Genetic ManipulationR01CA096512 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shou-Jiang Gao · 2003 to 2026
$7.4M
Roles of the K3 and K5 in KSHV Persistence and PathogenesisP01CA180779 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2013 to 2017
$7.3M
Molecular Basis of KSHV oncogenesisR35CA200422 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2016 to 2022
$6.1M
Role of UVRAG-mediated Autophagy in Tumor SuppressionR01CA140964 · NCI · WISTAR INSTITUTE · PI LIANG, CHENGYU · 2009 to 2025
$5.4M
Role of viral BCI-2 mediated anti-apoptosis and-autophagyR01AI073099 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2007 to 2017
$4.3M
KSHV Epigenetic RegulationR01DE023926 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JUNG, JAE U · 2013 to 2024
$4.2M
Mechanism of KSHV-induced angiogenesisR01CA132637 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GAO, SHOU-JIANG · 2008 to 2020
$3.6M
Targeting an immune kinase to purge KSHV latent infectionR01DE026003 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, CASEY, ZHANG, CHAO · 2016 to 2020
$3.4M
TRIM9-mediated anti-viral immune pathwayR01AI116585 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OU, J.-H. JAMES · 2015 to 2019
$2.3M
HISTONE MODIFIERS IN ORAL KSHV INFECTION AND MALIGNANCIESR01DE025465 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2015 to 2019
$2.0M
Targeting KSHV malignancies and persistent infectionR01CA197153 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2015 to 2019
$1.9M
KSHV microRNAs in tumor invasion and angiogenesisR01CA213275 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2017 to 2021
$959k
NCI NIH HHS P01 CA180779NCI NIH HHS R01 CA096512NCI NIH HHS R01 CA132637NCI NIH HHS R01 CA140964NCI NIH HHS R01 CA197153NCI NIH HHS R01 CA213275NCI NIH HHS R35 CA200422NIAID NIH HHS R01 AI073099NIAID NIH HHS R01 AI116585NIDCR NIH HHS R01 DE023926NIDCR NIH HHS R01 DE025465NIDCR NIH HHS R01 DE026003
6 · The paper itself

Abstract

The viral Bcl-2 homolog (vBcl2) of Kaposi's sarcoma-associated herpesvirus (KSHV) displays efficient antiapoptotic and antiautophagic activity through its central BH3 domain, which functions to prolong the life span of virus-infected cells and ultimately enhances virus replication and latency. Independent of its antiapoptotic and antiautophagic activity, vBcl2 also plays an essential role in KSHV lytic replication through its amino-terminal amino acids (aa) 11 to 20. Here, we report a novel molecular mechanism of vBcl2-mediated regulation of KSHV lytic replication. vBcl2 specifically bound the tegument protein open reading frame 55 (ORF55) through its amino-terminal aa 11 to 20, allowing their association with virions. Consequently, the vBcl2 peptide derived from vBcl2 aa 11 to 20 effectively disrupted the interaction between vBcl2 and ORF55, inhibiting the incorporation of the ORF55 tegument protein into virions. This study provides new insight into vBcl2's function in KSHV virion assembly that is separable from its inhibitory role in host apoptosis and autophagy.

Indexed as

Open Reading FramesVirus AssemblyApoptosisAutophagyBase SequenceDNA ReplicationDNA, ViralGene ExpressionGene Knockout TechniquesGenome, ViralHEK293 CellsHerpesvirus 8, HumanHumansOncogene ProteinsViral ProteinsBcl-2 protein, Human herpesvirus 8DNA, ViralOncogene ProteinsViral ProteinsautophagyKaposi's sarcoma-associated herpesvirusKSHVlytic replicationORF55 tegumentvBcl2virion assembly

Identifiers

PMID29167347
PMCPMC5790944
OpenAlexW2770375777

What Socratic 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 Socratic graph.