Evidence map›Paper›PMID 29040458›Full record

ArticlePathogens and disease2017

Orchestration of the mammalian host cell glucose transporter proteins-1 and 3 by Chlamydia contributes to intracellular growth and infectivity.

Xiaogang Wang, Kevin Hybiske, Richard S Stephens

Open access · bronzeAbstract read
In one paragraph

Article in Pathogens and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Molecular pathogenesis ofFrontiers in cellular and infection microbiology · 2023
    Review
  5. Article
  6. Article
  7. Insights Into Mitochondrial Dynamics in Chlamydial Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  8. Article
  9. Article
  10. Effect of Sugars onPathogens (Basel, Switzerland) · 2020
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Chlamydial Infection From Outside to Inside.Frontiers in microbiology · 2019
    Review
  16. 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

3 authors at 2 institutions in 1 country.

Xiaogang WangProgram in Infectious Diseases, School of Public Health, University of California, Berkeley, 51 Koshland Hall, CA 94720, USA.
Kevin HybiskeDivision of Allergy and Infectious Diseases, Department of Medicine, University of Washington, 750 Republican St, Seattle, WA 98109, USA.
Richard S StephensProgram in Infectious Diseases, School of Public Health, University of California, Berkeley, 51 Koshland Hall, CA 94720, USA.
University of California, Berkeley · USUniversity of Washington · US

Funding

Mechanisms of Host Cell Infection by ChlamydiaR01AI091851 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STEPHENS, RICHARD S · 2011 to 2015
$1.9M
NIAID NIH HHS R01 AI091851
6 · The paper itself

Abstract

Chlamydia are gram-negative obligate intracellular bacteria that replicate within a discrete cellular vacuole, called an inclusion. Although it is known that Chlamydia require essential nutrients from host cells to support their intracellular growth, the molecular mechanisms for acquiring these macromolecules remain uncharacterized. In the present study, it was found that the expression of mammalian cell glucose transporter proteins 1 (GLUT1) and glucose transporter proteins 3 (GLUT3) were up-regulated during chlamydial infection. Up-regulation was dependent on bacterial protein synthesis and Chlamydia-induced MAPK kinase activation. GLUT1, but not GLUT3, was observed in close proximity to the inclusion membrane throughout the chlamydial developmental cycle. The proximity of GLUT1 to the inclusion was dependent on a brefeldin A-sensitive pathway. Knockdown of GLUT1 and GLUT3 with specific siRNA significantly impaired chlamydial development and infectivity. It was discovered that the GLUT1 protein was stabilized during infection by inhibition of host-dependent ubiquitination of GLUT1, and this effect was associated with the chlamydial deubiquitinase effector protein CT868. This report demonstrates that Chlamydia exploits host-derived transporter proteins altering their expression, turnover and localization. Consequently, host cell transporter proteins are manipulated during infection as a transport system to fulfill the carbon source requirements for Chlamydia.

Indexed as

AnimalsCell LineChlamydia InfectionsChlamydia trachomatisGlucoseGlucose Transporter Type 1Glucose Transporter Type 3HeLa CellsHost-Pathogen InteractionsHumansInclusion BodiesMiceRNA InterferenceRNA, Small InterferingUbiquitinationUp-RegulationGlucoseGlucose Transporter Type 1Glucose Transporter Type 3RNA, Small InterferingSLC2A1 protein, humanSLC2A3 protein, humanglucose transporter proteinintracellular parasitepathogenesis

Identifiers

PMID29040458
PMCPMC6433302
OpenAlexW2760818404

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.