Evidence map›Paper›PMID 28482027›Full record

ArticleNucleic acids research2017

Cmr is a redox-responsive regulator of DosR that contributes to M. tuberculosis virulence.

Laura J Smith, Aleksandra Bochkareva, Matthew D Rolfe, Debbie M Hunt, Christina Kahramanoglou, Yvonne Braun, Angela Rodgers, Alix Blockley, Stephen Coade, Kathryn E A Lougheed and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 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
2.3field-weighted citation impact, top 12% 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, 31 citations in OpenAlex.

  1. cAMP-independent Crp homolog adds to the multi-layer regulatory network inFrontiers in cellular and infection microbiology · 2025
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  12. Microbiology spectrum · 2019
    Review
  13. Chemical disarming of isoniazid resistance inProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Article
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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

21 authors at 6 institutions in 2 countries.

Laura J SmithMolecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK.
Aleksandra BochkarevaMolecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK.
Matthew D RolfeMolecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK.
Debbie M HuntDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Christina KahramanoglouDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Yvonne BraunDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Angela RodgersDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Alix BlockleyDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Stephen CoadeDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Kathryn E A LougheedDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Nor Azian HafnehDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester LE1 9HN, UK.
Sarah M GlennDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester LE1 9HN, UK.
Jason C CrackCentre for Molecular and Structural Biochemistry, School of Chemistry, University of East Anglia, Norwich NR4 7TJ, UK.
Nick E Le BrunCentre for Molecular and Structural Biochemistry, School of Chemistry, University of East Anglia, Norwich NR4 7TJ, UK.
José W SaldanhaDivision of Mathematical Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Vadim MakarovA.N. Bach Institute of Biochemistry, Russian Academy of Sciences, Moscow, Russia.
Irene NobeliInstitute of Structural and Molecular Biology, Department of Biological Sciences, Birkbeck, University of London, Malet Street, London WC1E 7HX, UK.
Kristine ArnvigInstitute for Structural and Molecular Biology, University College London, London WC1E 6BT, UK.
Galina V MukamolovaDepartment of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester LE1 9HN, UK.
Roger S BuxtonDivision of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
Jeffrey GreenMolecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK.
University of Leicester · GBUniversity of Sheffield · GBInstitute of Structural and Molecular Biology · GBUniversity of East Anglia · GBA N Bach Institute of Biochemistry · RUDe Montfort University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/K000330/1Medical Research Council MC_U117585867
6 · The paper itself

Abstract

Mycobacterium tuberculosis (MTb) is the causative agent of pulmonary tuberculosis (TB). MTb colonizes the human lung, often entering a non-replicating state before progressing to life-threatening active infections. Transcriptional reprogramming is essential for TB pathogenesis. In vitro, Cmr (a member of the CRP/FNR super-family of transcription regulators) bound at a single DNA site to act as a dual regulator of cmr transcription and an activator of the divergent rv1676 gene. Transcriptional profiling and DNA-binding assays suggested that Cmr directly represses dosR expression. The DosR regulon is thought to be involved in establishing latent tuberculosis infections in response to hypoxia and nitric oxide. Accordingly, DNA-binding by Cmr was severely impaired by nitrosation. A cmr mutant was better able to survive a nitrosative stress challenge but was attenuated in a mouse aerosol infection model. The complemented mutant exhibited a ∼2-fold increase in cmr expression, which led to increased sensitivity to nitrosative stress. This, and the inability to restore wild-type behaviour in the infection model, suggests that precise regulation of the cmr locus, which is associated with Region of Difference 150 in hypervirulent Beijing strains of Mtb, is important for TB pathogenesis.

Indexed as

AnimalsBacterial ProteinsCells, CulturedDNA-Binding ProteinsEscherichia coliFemaleGene Expression Regulation, BacterialMacrophagesMice, Inbred BALB CMycobacterium smegmatisMycobacterium tuberculosisOxidation-ReductionProtein BindingProtein KinasesTranscription FactorsTranscription, GeneticBacterial ProteinsDNA-Binding ProteinsDosR protein, Mycobacterium tuberculosisProtein KinasesTranscription FactorsVirulence Factors

Identifiers

PMID28482027
PMCPMC5499769
OpenAlexW2612583181

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.