Evidence map›Paper›PMID 28459842›Full record

ArticlePLoS pathogens2017

Phosphorylated STAT5 directly facilitates parvovirus B19 DNA replication in human erythroid progenitors through interaction with the MCM complex.

Safder S Ganaie, Wei Zou, Peng Xu, Xuefeng Deng, Steve Kleiboeker, Jianming Qiu

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 44 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

6 authors at 2 institutions in 1 country.

Safder S GanaieDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Wei ZouDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Peng XuDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Xuefeng DengDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, United States of America.
Steve KleiboekerDepartment of Research and Development, Viracor Eurofins Laboratories, Lee's Summit, Missouri, United States of America.
Jianming QiuDepartment of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas, United States of America.ORCID http://orcid.org/0000-0001-9850-1695
University of Kansas Medical Center · USEurofins (United States) · US

Funding

Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Post-Transcriptional Regulation of Parvovirus Capsid Gene ExpressionR01AI070723 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI QIU, JIANMING · 2007 to 2017
$3.3M
Post-Transcriptional Regulation of Parvovirus Capsid Gene ExpressionR56AI070723 · NIAID · UNIVERSITY OF KANSAS MEDICAL CENTER · PI QIU, JIANMING · 2006 to 2006
$290k
NIAID NIH HHS R01 AI070723NIAID NIH HHS R56 AI070723NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

Productive infection of human parvovirus B19 (B19V) exhibits high tropism for burst forming unit erythroid (BFU-E) and colony forming unit erythroid (CFU-E) progenitor cells in human bone marrow and fetal liver. This exclusive restriction of the virus replication to human erythroid progenitor cells is partly due to the intracellular factors that are essential for viral DNA replication, including erythropoietin signaling. Efficient B19V replication also requires hypoxic conditions, which upregulate the signal transducer and activator of transcription 5 (STAT5) pathway, and phosphorylated STAT5 is essential for virus replication. In this study, our results revealed direct involvement of STAT5 in B19V DNA replication. Consensus STAT5-binding elements were identified adjacent to the NS1-binding element within the minimal origins of viral DNA replication in the B19V genome. Phosphorylated STAT5 specifically interacted with viral DNA replication origins both in vivo and in vitro, and was actively recruited within the viral DNA replication centers. Notably, STAT5 interacted with minichromosome maintenance (MCM) complex, suggesting that STAT5 directly facilitates viral DNA replication by recruiting the helicase complex of the cellular DNA replication machinery to viral DNA replication centers. The FDA-approved drug pimozide dephosphorylates STAT5, and it inhibited B19V replication in ex vivo expanded human erythroid progenitors. Our results demonstrated that pimozide could be a promising antiviral drug for treatment of B19V-related diseases.

Indexed as

DNA ReplicationVirus ReplicationErythroid Precursor CellsErythropoietinHumansMinichromosome Maintenance ProteinsParvovirus B19, HumanPhosphorylationSignal TransductionSTAT5 Transcription FactorErythropoietinMinichromosome Maintenance ProteinsSTAT5 Transcription Factor

Identifiers

PMID28459842
PMCPMC5426800
OpenAlexW2611074608

What Socratic holds

Textmetadata
LicenceCC BY
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.