Evidence map›Paper›PMID 27932618›Full record

ArticleThe Journal of infectious diseases2017

The Roles of Unfolded Protein Response Pathways in Chlamydia Pathogenesis.

Zenas George, Yusuf Omosun, Anthony A Azenabor, James Partin, Kahaliah Joseph, Debra Ellerson, Qing He, Francis Eko, Claudiu Bandea, Pavel Svoboda and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024
    Review
  6. Article
  7. Journal of immunology research · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The Journal of biological chemistry · 2020
    Article
  16. Article
  17. The molecular mechanism of induction of unfolded protein response by Chlamydia.Biochemical and biophysical research communications · 2019
    Article
  18. Review
  19. Annals of the rheumatic diseases · 2019
    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

13 authors at 2 institutions in 1 country.

Zenas GeorgeCenters for Disease Control and Prevention, and.
Yusuf OmosunCenters for Disease Control and Prevention, and.
Anthony A AzenaborDepartment of Biomedical Sciences, University of Wisconsin, Milwaukee.
James PartinCenters for Disease Control and Prevention, and.
Kahaliah JosephCenters for Disease Control and Prevention, and.
Debra EllersonCenters for Disease Control and Prevention, and.
Qing HeCenters for Disease Control and Prevention, and.
Francis EkoDepartment of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine, Atlanta, Georgia.
Claudiu BandeaCenters for Disease Control and Prevention, and.
Pavel SvobodaCenters for Disease Control and Prevention, and.
Jan PohlCenters for Disease Control and Prevention, and.
Carolyn M BlackCenters for Disease Control and Prevention, and.
Joseph U IgietsemeCenters for Disease Control and Prevention, and.
Morehouse School of Medicine · USUniversity of Wisconsin–Milwaukee · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chlamydia is an obligate intracellular bacterium that relies on host cells for essential nutrients and adenosine triphosphate (ATP) for a productive infection. Although the unfolded protein response (UPR) plays a major role in certain microbial infectivity, its role in chlamydial pathogenesis is unknown. We hypothesized that Chlamydia induces UPR and exploits it to upregulate host cell uptake and metabolism of glucose, production of ATP, phospholipids, and other molecules required for its replicative development and host survival. Using a combination of biochemical and pathway inhibition assays, we showed that the 3 UPR pathway transducers-protein kinase RNA-activated (PKR)-like ER kinase (PERK), inositol-requiring enzyme-1α (IRE1α), and activating transcription factor-6α (ATF6α)-were activated during Chlamydia infection. The kinase activity of PERK and ribonuclease (RNase) of IRE1α mediated the upregulation of hexokinase II and production of ATP via substrate-level phosphorylation. In addition, the activation of PERK and IRE1α promoted autophagy formation and apoptosis resistance for host survival. Moreover, the activation of IRE1α resulted in the generation of spliced X-box binding protein 1 (sXBP1) and upregulation of lipid production. The vital role of UPR pathways in Chlamydia development and pathogenesis could lead to the identification of potential molecular targets for therapeutics against Chlamydia.

Indexed as

Unfolded Protein ResponseActivating Transcription Factor 6AnimalsApoptosisCell SurvivalChlamydiaChlamydia InfectionseIF-2 KinaseEndoribonucleasesEnzyme ActivationFemaleMiceMice, Inbred C57BLProtein Serine-Threonine KinasesSignal TransductionActivating Transcription Factor 6Atf6 protein, mouseeIF-2 KinaseEndoribonucleasesErn1 protein, mouseProtein Serine-Threonine KinasesChlamydiapathogenesisunfolded protein response.

Identifiers

PMID27932618
PMCPMC6455037
OpenAlexW2560103880

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.