Evidence map›Paper›PMID 31974609›Full record

ArticleMolecular medicine reports2020

Carboxyl terminal activating region 3 of latent membrane protein 1 encoded by the Epstein‑Barr virus regulates cell proliferation and protein expression in NP69 cells.

Zhi-Wei Zhang, He-Liang Zhang, Yan-Hui Yu, Yong-Mei Ouyang, Zhu-Chu Chen, Xiu-Sheng He, Zhi-Min He

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

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Review
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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 2 institutions in 1 country.

Zhi-Wei ZhangCancer Research Institute of Medical College, University of South China, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan, Hengyang, Hunan 421001, P.R. China.
He-Liang ZhangCancer Research Institute of Medical College, University of South China, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan, Hengyang, Hunan 421001, P.R. China.
Yan-Hui YuCancer Research Institute, Central South University, Xiangya School of Medicine, Changsha, Hunan 410078, P.R. China.
Yong-Mei OuyangCancer Research Institute, Central South University, Xiangya School of Medicine, Changsha, Hunan 410078, P.R. China.
Zhu-Chu ChenCancer Research Institute, Central South University, Xiangya School of Medicine, Changsha, Hunan 410078, P.R. China.
Xiu-Sheng HeCancer Research Institute of Medical College, University of South China, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan, Hengyang, Hunan 421001, P.R. China.
Zhi-Min HeCancer Research Institute, Central South University, Xiangya School of Medicine, Changsha, Hunan 410078, P.R. China.
Central South University · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, the mechanism by which carboxyl terminal activating region 3 (CTAR3) of latent membrane protein 1 (LMP1), encoded by the Epstein‑Barr virus, regulated cell proliferation and protein expression was investigated in the nasopharyngeal epithelial cell line NP69. The deletion mutant LMP1 (LMP1Δ232‑351; amino acid residues including 232‑351 codons in CTAR3 deleted) was generated by polymerase chain reaction. An NP69‑LMP1Δ232‑351 cell line was established by retroviral infection. Finally, cell proliferation and protein expression of NP69 cells expressing LMP1Δ232‑351 were examined using a cell growth curve and western blot analysis. The results demonstrated: i) The proliferation of NP69‑LMP1Δ232‑351 cells was significantly decreased compared with cells expressing wild type LMP1 (LMP1WT; n=3; P<0.05); ii) 17 proteins exhibited differential protein expression (>2‑fold change) in NP69‑LMP1Δ232‑351 cells compared with NP69‑LMP1WT cells; and iii) LMP1WT was involved in activating the Janus kinase 3 (JAK3) promoter and regulating the expression of JAK3 protein, while LMP1Δ232‑351 was almost defective in ability to activate the JAK promoter. These results suggested that LMP1‑CTAR3 may be an important functional domain for regulating cell proliferation and protein expression in nasopharyngeal epithelial cells.

Indexed as

Cell Line, TumorCell ProliferationHerpesvirus 4, HumanHeterogeneous-Nuclear RibonucleoproteinsHumansJanus Kinase 3PlasmidsPromoter Regions, GeneticProtein DomainsProton-Motive ForceReproducibility of ResultsSignal TransductionStructure-Activity RelationshipTranscription, GeneticViral Matrix ProteinsEBV-associated membrane antigen, Epstein-Barr virusHeterogeneous-Nuclear RibonucleoproteinsJAK3 protein, humanJanus Kinase 3Viral Matrix Proteinscarboxyl terminal activating region 3cell proliferationJanus kinase 3latent membrane protein 1nP69proteome

Identifiers

PMID31974609
PMCPMC6947836
OpenAlexW2994005170

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.