Evidence map›Paper›PMID 30787154›Full record

ArticleJournal of virology2019

Marek's Disease Virus Disables the ATR-Chk1 Pathway by Activating STAT3.

Xue Lian, Chenyi Bao, Xueqi Li, Xunhai Zhang, Hongjun Chen, Yong-Sam Jung, Yingjuan Qian

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025
    Review
  3. Article
  4. Article
  5. 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

7 authors at 3 institutions in 1 country.

Xue LianMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Chenyi BaoMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Xueqi LiMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Xunhai ZhangAnhui Provincial Key Laboratory for Control and Monitoring of Poultry Diseases, Anhui Science and Technology University, Fengyang, China.
Hongjun ChenShanghai Veterinary Research Institute, Chinese Academic of Agricultural Sciences, Shanghai, China.
Yong-Sam JungMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.ORCID 0000-0003-0324-162X
Yingjuan QianMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China yqian@njau.edu.cn.
Nanjing Agricultural University · CNAnhui University of Science and Technology · CNShanghai Veterinary Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogenic virus replication often leads to genomic instability, causing DNA damage and inducing the DNA damage response (DDR) pathway. The DDR pathway is a cellular pathway that senses DNA damage and regulates the cell cycle to maintain genomic stability. Therefore, the DDR pathway is critical for the viral lifecycle and tumorigenesis. Marek's disease virus (MDV), an alphaherpesvirus that causes lymphoma in chickens, has been shown to induce DNA damage in infected cells. However, the interaction between MDV and the host DDR is unclear. In this study, we observed that MDV infection causes DNA strand breakage in chicken fibroblast (CEF) cells along with an increase in the DNA damage markers p53 and p21. Interestingly, we showed that phosphorylation of STAT3 was increased during MDV infection, concomitantly with a decrease of Chk1 phosphorylation. In addition, we found that MDV infection was enhanced by VE-821, an ATR-specific inhibitor, but attenuated by hydroxyurea, an ATR activator. Moreover, inhibition of STAT3 phosphorylation by Stattic eliminates the ability of MDV to inhibit Chk1 phosphorylation. Finally, we showed that MDV replication was decreased by Stattic treatment. Taken together, these results suggest that MDV disables the ATR-Chk1 pathway through STAT3 activation to benefit its replication.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsAvian ProteinsCell LineCheckpoint Kinase 1ChickensCyclin-Dependent Kinase Inhibitor p21DNA DamageMardivirusMarek DiseasePyrazinesSTAT3 Transcription FactorSulfonesTumor Suppressor Protein p53Virus Replication3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamideAtaxia Telangiectasia Mutated ProteinsAvian ProteinsCheckpoint Kinase 1Cyclin-Dependent Kinase Inhibitor p21PyrazinesSTAT3 Transcription FactorSulfonesTumor Suppressor Protein p53ATR-Chk1 pathwayDNA damageMarek's disease virusSTAT3viral replication

Identifiers

PMID30787154
PMCPMC6475774
OpenAlexW2917306314

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.