Evidence map›Paper›PMID 35913163›Full record

ArticlemBio2022

CroR Regulates Expression of

Sarah B Timmler, Stephanie L Kellogg, Samantha N Atkinson, Jaime L Little, Dušanka Djorić, Christopher J Kristich

Open access · goldAbstract read
In one paragraph

Article in mBio, 2022. 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
1.8field-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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. A two-component system signaling hub controls enterococcal membrane remodeling in response to daptomycin.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  5. Article
  6. Article
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  9. Article
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  11. Review
  12. Article
  13. Article
  14. Non-Clinical microbiology reviews · 2024
    Review
  15. Article
  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

6 authors at 1 institution in 1 country.

Sarah B TimmlerDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.
Stephanie L KelloggDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.
Samantha N AtkinsonDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.
Jaime L LittleDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.
Dušanka DjorićDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.
Christopher J KristichDepartment of Microbiology and Immunology, Medical College of Wisconsingrid.30760.32, Milwaukee, Wisconsin, USA.ORCID 0000-0002-1660-0006
Medical College of Wisconsin · US

Funding

Role and regulation of peptidoglycan synthases in enterococcal antimicrobial resistanceR01AI150895 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI KRISTICH, CHRISTOPHER J · 2020 to 2024
$2.4M
Intrinsic cephalosporin resistance in enterococciR01AI134660 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI KRISTICH, CHRISTOPHER J · 2018 to 2021
$1.5M
Host factors required for vancomycin resistance in enterococciR21AI153391 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI KRISTICH, CHRISTOPHER J · 2021 to 2022
$429k
NIAID NIH HHS R01 AI134660NIAID NIH HHS R01 AI150895NIAID NIH HHS R21 AI153391
6 · The paper itself

Abstract

Enterococcus faecalis is an opportunistic pathogen and a major cause of severe nosocomial infections. Treatment options against enterococcal infections are declining due to the resistance of enterococci to numerous antibiotics. A key risk factor for developing enterococcal infections is treatment with cephalosporin antibiotics, to which enterococci are intrinsically resistant. For susceptible organisms, cephalosporins inhibit bacterial growth by acylating the active site of penicillin-binding proteins (PBPs), key enzymes that catalyze peptidoglycan cross-linking. Two specific PBPs of enterococci, Pbp4(5) and PbpA(2b), exhibit low reactivity toward cephalosporins, allowing these PBPs to cross-link peptidoglycan in the presence of cephalosporins to drive resistance in enterococci, but the mechanisms by which these PBPs are regulated are poorly understood. The CroS/R two-component signal transduction system (TCS) is also required for cephalosporin resistance. Activation of CroS/R by cephalosporins leads to CroR-dependent changes in gene expression. However, the specific genes regulated by CroS/R that are responsible for cephalosporin resistance remain largely unknown. In this study, we characterized CroR-dependent transcriptome remodeling by RNA-seq, identifying

Indexed as

Cephalosporin ResistanceEnterococcus faecalisAnti-Bacterial AgentsBacterial ProteinsCephalosporinsMicrobial Sensitivity TestsPenicillin-Binding ProteinsPeptidoglycanAnti-Bacterial AgentsBacterial ProteinsCephalosporinsPenicillin-Binding ProteinsPeptidoglycancephalosporin resistanceCroREnterococcusPbp4Pbp4(5)two-component signaling system

Identifiers

PMID35913163
PMCPMC9426447
OpenAlexW4289313607

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.