Evidence map›Paper›PMID 16150462›Full record

ArticleLife sciences2005

Phosphorylation of PI3K/Akt and MAPK/ERK in an early entry step of enterovirus 71.

Wen-Rou Wong, Yu-Yun Chen, Shun-Min Yang, Yin-Li Chen, Jim-Tong Horng

Abstract read
In one paragraph

Article in Life sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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

49 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors.

Wen-Rou WongDepartment of Dermatology, Chang Gung Memorial Hospital, 199 Tung-Hwa North Road, Taipei 105, Taiwan.
Yu-Yun Chen
Shun-Min Yang
Yin-Li Chen
Jim-Tong Horng

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viruses have been known to subvert the anti-apoptotic pathways of the host cell in order to delay apoptosis. However, the mechanisms utilized by enterovirus 71 (EV71) to mediate anti-apoptotic activity remained undetermined. We observed that EV71 infection induced an early activation of both phosphatidylinositol 3-kinase (PI3K)/Akt and MAPK/ERK signaling pathways. The activity of GSK3beta, a downstream target of these pathways, was negatively regulated by the activation of both MAPK/ERK and PI3K/Akt. The phosphorylation of GSK3 could be inhibited by treatment with the specific inhibitors of MAPK/ERK and PI3K/Akt. Other Akt downstream targets, BAD, caspase-9 and the Forkhead transcription factor (FKHR), were not phosphorylated during the course of infection by EV71. We further demonstrated that infection by UV-irradiated, inactivated virus triggered early Akt activation but was insufficient to trigger late Akt activation. These data suggest that with the phosphorylation of MAPK/ERK and PI3K/Akt the subsequent inactivation of GSK3beta is utilized by EV71 as a potential mechanism to delay host cell apoptosis.

Indexed as

EnterovirusAnimalsbcl-Associated Death ProteinBlotting, WesternCaspase 9CaspasesCells, CulturedChlorocebus aethiopsElectrophoresisEnterovirus InfectionsEnzyme ActivationMitogen-Activated Protein KinasesOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphorylationUltraviolet Raysbcl-Associated Death ProteinCaspase 9CaspasesMitogen-Activated Protein KinasesOncogene Protein v-aktPhosphatidylinositol 3-Kinases

Identifiers

PMID16150462
PMCPMC7094582

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.