Evidence map›Paper›PMID 26883353›Full record

ArticleMolecular and cellular pediatrics2016

Diverse roles of endoplasmic reticulum stress sensors in bacterial infection.

Helena Pillich, Maria Loose, Klaus-Peter Zimmer, Trinad Chakraborty

Open access · goldAbstract read
In one paragraph

Article in Molecular and cellular pediatrics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Infection and immunity · 2026
    Article
  2. bioRxiv : the preprint server for biology · 2026
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  12. Toll-like receptor 2 (TLR2) engages endoplasmic reticulum stress sensor IRE1α to regulate retinal innate responses in Staphylococcus aureus endophthalmitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Article
  14. The Journal of biological chemistry · 2020
    Article
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  19. Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019
    Review
  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

4 authors at 1 institution in 1 country.

Helena PillichInstitute of Medical Microbiology, Justus-Liebig-University Giessen, 35392, Giessen, Germany. Helena.Pillich@mikrobio.med.uni-giessen.de.
Maria LooseInstitute of Medical Microbiology, Justus-Liebig-University Giessen, 35392, Giessen, Germany. Maria.Loose@mikrobio.med.uni-giessen.de.
Klaus-Peter ZimmerDepartment of Pediatrics, Justus-Liebig-University Giessen, 35392, Giessen, Germany. Klaus-Peter.Zimmer@paediat.med.uni-giessen.de.
Trinad ChakrabortyInstitute of Medical Microbiology, Justus-Liebig-University Giessen, 35392, Giessen, Germany. Trinad.Chakraborty@mikrobio.med.uni-giessen.de.
University of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial infection often leads to cellular damage, primarily marked by loss of cellular integrity and cell death. However, in recent years, it is being increasingly recognized that, in individual cells, there are graded responses collectively termed cell-autonomous defense mechanisms that induce cellular processes designed to limit cell damage, enable repair, and eliminate bacteria. Many of these responses are triggered not by detection of a particular bacterial effector or ligand but rather by their effects on key cellular processes and changes in homeostasis induced by microbial effectors when recognized. These in turn lead to a decrease in essential cellular functions such as protein translation or mitochondrial respiration and the induction of innate immune responses that may be specific to the cellular deficit induced. These processes are often associated with specific cell compartments, e.g., the endoplasmic reticulum (ER). Under non-infection conditions, these systems are generally involved in sensing cellular stress and in inducing and orchestrating the subsequent cellular response. Thus, perturbations of ER homeostasis result in accumulation of unfolded proteins which are detected by ER stress sensors in order to restore the normal condition. The ER is also important during bacterial infection, and bacterial effectors that activate the ER stress sensors have been discovered. Increasing evidence now indicate that bacteria have evolved strategies to differentially activate different arms of ER stress sensors resulting in specific host cell response. In this review, we will describe the mechanisms used by bacteria to activate the ER stress sensors and discuss their role during infection.

Indexed as

Bacterial effectorsBacterial infectionEndoplasmic reticulum stress

Identifiers

PMID26883353
PMCPMC4755955
OpenAlexW2297601881

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.