Evidence map›Paper›PMID 28803120›Full record

ArticleEBioMedicine2017

Chlamydia trachomatis Prevents Apoptosis Via Activation of PDPK1-MYC and Enhanced Mitochondrial Binding of Hexokinase II.

Munir A Al-Zeer, Audrey Xavier, Mohammad Abu Lubad, Janine Sigulla, Mirjana Kessler, Robert Hurwitz, Thomas F Meyer

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  4. c-Myc inhibits macrophage antimycobacterial response inbioRxiv : the preprint server for biology · 2025
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  7. Microorganisms · 2023
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  9. Article
  10. Article
  11. Article
  12. Article
  13. Loss of p53 Expression in Gastric Epithelial Cells ofInternational journal of microbiology · 2022
    Article
  14. Review
  15. Insights Into Mitochondrial Dynamics in Chlamydial Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  16. Review
  17. Review
  18. Journal of Cancer · 2021
    Review
  19. Article
  20. Hijacking and Use of Host Kinases by Chlamydiae.Pathogens (Basel, Switzerland) · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Munir A Al-ZeerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany. Electronic address: al-zeer@mpiib-berlin.mpg.de.
Audrey XavierDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany; The Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Mohammad Abu LubadDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany; Mu'tah University, Faculty of Medicine, Al-Karak, Jordan.
Janine SigullaDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Mirjana KesslerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Robert HurwitzProtein Purification Core Facility, Max Planck Institute for Infection Biology, Berlin, Germany.
Thomas F MeyerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany. Electronic address: meyer@mpiib-berlin.mpg.de.
Max Planck Institute for Infection Biology · DEMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intracellular human bacterial pathogen Chlamydia trachomatis pursues effective strategies to protect infected cells against death-inducing stimuli. Here, we show that Chlamydia trachomatis infection evokes 3-phosphoinositide-dependent protein kinase-1 (PDPK1) signaling to ensure the completion of its developmental cycle, further leading to the phosphorylation and stabilization of MYC. Using biochemical approaches and imaging we demonstrate that Chlamydia-induced PDPK1-MYC signaling induces host hexokinase II (HKII), which becomes enriched and translocated to the mitochondria. Strikingly, preventing the HKII interaction with mitochondria using exogenous peptides triggers apoptosis of infected cells as does inhibiting either PDPK1 or MYC, which also disrupts intracellular development of Chlamydia trachomatis. These findings identify a previously unknown pathway activated by Chlamydia infection, which exhibits pro-carcinogenic features. Targeting the PDPK1-MYC-HKII-axis may provide a strategy to overcome therapeutic resistance of infection.

Indexed as

Apoptosis3-Phosphoinositide-Dependent Protein KinasesChlamydia InfectionsChlamydia trachomatisEnzyme ActivationHeLa CellsHexokinaseHost-Pathogen InteractionsHumansImmunohistochemistryMitochondriaPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-myc3-Phosphoinositide-Dependent Protein KinasesHexokinasePDPK1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-mycHost-pathogen interactionMetabolismMYCPDPK1Warburg effect

Identifiers

PMID28803120
PMCPMC5605330
OpenAlexW2745238181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.