Evidence map›Paper›PMID 25136516›Full record

ReviewFrontiers in cellular and infection microbiology2014

Induction of endoplasmic reticulum stress and unfolded protein response constitutes a pathogenic strategy of group A streptococcus.

Moshe Baruch, Baruch B Hertzog, Miriam Ravins, Aparna Anand, Catherine Youting Cheng, Debabrata Biswas, Boaz Tirosh, Emanuel Hanski

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Science advances · 2026
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  4. Induction of the ISR by AB5 subtilase cytotoxin drives type-I IFN expression in pDCs via STING activation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Non-canonical activation of IRE1α duringbioRxiv : the preprint server for biology · 2024
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  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Journal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

8 authors at 2 institutions in 2 countries.

Moshe BaruchDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel.
Baruch B HertzogDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel.
Miriam RavinsDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel.
Aparna AnandDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel.
Catherine Youting ChengDepartment of Microbiology, Center for Research Excellence and Technological Enterprise (CREATE), National University of Singapore (NUS) and NUS-HUJI Singapore.
Debabrata BiswasDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel ; Department of Microbiology, Center for Research Excellence and Technological Enterprise (CREATE), National University of Singapore (NUS) and NUS-HUJI Singapore.
Boaz TiroshThe School of Pharmacy, Institute for Drug Research, The Hebrew University of Jerusalem Jerusalem, Israel.
Emanuel HanskiDepartment of Microbiology and Molecular Genetics, Faculty of Medicine, The Hebrew University of Jerusalem (HUJI) Jerusalem, Israel ; Department of Microbiology, Center for Research Excellence and Technological Enterprise (CREATE), National University of Singapore (NUS) and NUS-HUJI Singapore.
Hebrew University of Jerusalem · ILSingapore-HUJ Alliance for Research and Enterprise · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The connection between bacterial pathogens and unfolded protein response (UPR) is poorly explored. In this review we highlight the evidence showing that group A streptococcus (GAS) induces endoplasmic reticulum (ER) stress and UPR through which it captures the amino acid asparagine (ASN) from the host. GAS acts extracellularly and during adherence to host cells it delivers the hemolysin toxins; streptolysin O (SLO) and streptolysin S (SLS). By poorly understood pathways, these toxins trigger UPR leading to the induction of the transcriptional regulator ATF4 and consequently to the upregulation of asparagine synthetase (ASNS) transcription leading to production and release of ASN. GAS senses ASN and alters gene expression profile accordingly, and increases the rate of multiplication. We suggest that induction of UPR by GAS and by other bacterial pathogens represent means through which bacterial pathogens gain nutrients from the host, obviating the need to become internalized or inflict irreversible cell damage.

Indexed as

Endoplasmic Reticulum StressUnfolded Protein ResponseAnimalsAsparagineBacterial ProteinsHost-Pathogen InteractionsHumansStreptococcal InfectionsStreptococcus pyogenesStreptolysinsAsparagineBacterial Proteinsstreptolysin Ostreptolysin SStreptolysinsasparaginaseasparaginegroup A streptococcusmetabolismUPRvirulence

Identifiers

PMID25136516
PMCPMC4120759
OpenAlexW2162580275

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.