Evidence map›Paper›PMID 31934113›Full record

ArticleInternational journal of clinical and experimental pathology2019

IE86 Inhibits the apoptosis and promotes the cell proliferation of glioma cells via the hnRNP A2/B1-mediated alternative splicing of Bcl-x.

Rou Zhao, Ming Hu, Shuzhen Liang, Bin Wang, Bo Yu, Guimei Yang, Dongmeng Qian

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Critical Role of RNA mCellular and molecular neurobiology · 2023
    Review
  5. Review
  6. Review
  7. Aberrant Bcl-x splicing in cancer: from molecular mechanism to therapeutic modulation.Journal of experimental & clinical cancer research : CR · 2021
    Review
  8. Apoptosis Disorder, a Key Pathogenesis of HCMV-Related Diseases.International journal of molecular sciences · 2021
    Review
  9. Tuning the Orchestra: HCMV vs. Innate Immunity.Frontiers in microbiology · 2020
    Review
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.

Rou ZhaoDepartment of Microbiology, Qingdao University Life Science College Qingdao, Shandong, P. R. China.
Ming HuBasic Medical College, Qingdao University Medical College Qingdao, Shandong, P. R. China.
Shuzhen LiangBasic Medical College, Qingdao University Medical College Qingdao, Shandong, P. R. China.
Bin WangBasic Medical College, Qingdao University Medical College Qingdao, Shandong, P. R. China.
Bo YuBasic Medical College, Qingdao University Medical College Qingdao, Shandong, P. R. China.
Guimei YangSecond Affiliated Hospital of Shandong University of Traditional Chinese Medicine Jinan, Shandong, P. R. China.
Dongmeng QianDepartment of Microbiology, Qingdao University Life Science College Qingdao, Shandong, P. R. China.
Qingdao University · CNShandong University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cytomegalovirus (HCMV), a ubiquitous pathogen, can cause severe illness in immunocompromised individuals. Typically, glioma is one of the most common malignant primary brain tumors and originates in the central nervous system. The IE86 gene of HCMV exerts a major role in regulating virus replication. By using coimmunoprecipitation combined with mass spectrometry, the components of the IE86 complex were identified, and the heterogeneous ribonucleoprotein A2/B1 (hnRNP A2/B1) was recognized as one of the IE86 complex components. hnRNP A2/B1 is highly expressed in U251 cells, and the data suggest that IE86 can promote hnRNP A2/B1 expression. Furthermore, the knockdown of hnRNP A2/B1 significantly attenuates IE86-mediated apoptosis and cell proliferation. Importantly, IE86 can also inhibit the alternative splicing of Bcl-x by decreasing the Bcl-xS/Bcl-xL ratio, which is closely related to apoptosis. Meanwhile, the knockdown of hnRNP A2/B1 can mitigate the inhibitory effect of IE86 on the alternative splicing of Bcl-x. In conclusion, the inhibition of apoptosis and enhancement of cell proliferation by IE86 may be related to the hnRNP A2/B1-mediated alternative splicing of Bcl-x.

Indexed as

Bcl-xhnRNP A2/B1IE86

Identifiers

PMID31934113
PMCPMC6949557
OpenAlexW3016028790

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.