Evidence map›Paper›PMID 24103776›Full record

ArticleMolecular oral microbiology2014

Cnm is a major virulence factor of invasive Streptococcus mutans and part of a conserved three-gene locus.

A Avilés-Reyes, J H Miller, P J Simpson-Haidaris, J A Lemos, J Abranches

Abstract read
In one paragraph

Article in Molecular oral microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. TheApplied and environmental microbiology · 2026
    Article
  2. Raman signatures ofFrontiers in microbiology · 2026
    Article
  3. Raman signatures ofFrontiers in microbiology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Risk Assessment of Cnm-PositiveFrontiers in neurology · 2022
    Article
  11. Article
  12. Antibiotics (Basel, Switzerland) · 2021
    Article
  13. Virulence · 2020
    Article
  14. Article
  15. Article
  16. Inactivation ofJournal of oral microbiology · 2019
    Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

A Avilés-ReyesCenter for Oral Biology, University of Rochester Medical Center, Rochester, NY, USA; Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY, USA.
J H Miller
P J Simpson-Haidaris
J A Lemos
J Abranches
University of Rochester Medical Center · US

Funding

Training Program in Oral ScienceT90DE021985 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE, YULE, DAVID I · 2011 to 2021
$5.6M
Intracellular Invasion by Streptococcus mutans: Significance in DiseaseR01DE022559 · NIDCR · UNIVERSITY OF ROCHESTER · PI Jacqueline Abranches, Christine M. Szymanski · 2013 to 2026
$4.8M
NIDCR NIH HHS R01 DE022559NIDCR NIH HHS T90 DE021985
6 · The paper itself

Abstract

Cnm, a collagen- and laminin-binding protein present in a subset of Streptococcus mutans strains, mediates binding to extracellular matrices (ECM), intracellular invasion and virulence in the Galleria mellonella model. Antibodies raised against Cnm were used to confirm expression and the cell surface localization of Cnm in the highly invasive OMZ175 strain. Sequence analysis identified two additional genes (cnaB and cbpA) encoding putative surface proteins immediately upstream of cnm. Inactivation of cnaB and cbpA in OMZ175, individually or in combination, did not decrease the ability of this highly invasive and virulent strain to bind to different ECM proteins, invade human coronary artery endothelial cells (HCAEC), or kill G. mellonella. Similarly, expression of cnaB and cbpA in the cnm(-) strain UA159 revealed that these genes did not enhance Cnm-related phenotypes. However, integration of cnm in the chromosome of UA159 significantly increased its ability to bind to collagen and laminin, invade HCAEC, and kill G. mellonella. Moreover, the presence of antibodies against Cnm nearly abolished the ability of OMZ175 to bind to collagen and laminin and invade HCAEC, and significantly protected G. mellonella against OMZ175 infection. We concluded that neither CnaB nor CbpA is necessary for the expression of Cnm-related traits. We also provided definitive evidence that Cnm is an important virulence factor and a suitable target for the development of novel preventive and therapeutic strategies to combat invasive S. mutans strains.

Indexed as

Adhesins, BacterialAnimalsAntibodies, BacterialBacterial AdhesionBacterial ProteinsCarrier ProteinsCell LineCollagenEndothelial CellsExtracellular MatrixGenetic LociHumansLamininMembrane ProteinsMothsStreptococcal InfectionsAdhesins, BacterialAntibodies, BacterialBacterial ProteinsCarrier ProteinsCnm protein, Streptococcus mutansCollagenLamininMembrane ProteinsVirulence FactorsCnmcollagen-binding proteinintracellular invasionStreptococcus mutans

Identifiers

PMID24103776
PMCPMC3982401
OpenAlexW2025009418

What OpenQuestion holds

Textmetadata
LicenceTDM
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.