Evidence map›Paper›PMID 17339363›Full record

ArticleInfection and immunity2007

Mucosal tissue invasion by Candida albicans is associated with E-cadherin degradation, mediated by transcription factor Rim101p and protease Sap5p.

C C Villar, H Kashleva, C J Nobile, A P Mitchell, A Dongari-Bagtzoglou

Abstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

104 citing papers in PubMed, 195 citations in OpenAlex.

  1. Persistent, Asymptomatic Colonization withMicrobiology spectrum · 2022
    Trial
  2. Article
  3. Review
  4. Review
  5. Secreted Aspartic Proteinases: Key Factors inInternational journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Interkingdom assemblages in human saliva display group-level surface mobility and disease-promoting emergent functions.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Review

44 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

C C VillarDepartment of Periodontology, School of Dental Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1710, USA. cvillar@uchc.edu
H Kashleva
C J Nobile
A P Mitchell
A Dongari-Bagtzoglou
University of Connecticut · USColumbia University · US

Funding

Oral Epithelial Cells, Candida and PMN ActivationR01DE013986 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI Anna I Dongari-Bagtzoglou · 2000 to 2026
$9.2M
Genetic Control of Entry into Meiosis in YeastR01AI070272 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MITCHELL, AARON P · 2006 to 2010
$1.9M
NIAID NIH HHS 9R01 AI070272NIAID NIH HHS R01 AI070272NIDCR NIH HHS 2R01 DE13986NIDCR NIH HHS R01 DE013986
6 · The paper itself

Abstract

The ability of Candida albicans to invade mucosal tissues is a major virulence determinant of this organism; however, the mechanism of invasion is not understood in detail. Proteolytic breakdown of E-cadherin, the major protein in epithelial cell junctions, has been proposed as a mechanism of invasion of certain bacteria in the oral mucosa. The objectives of this study were (i) to assess whether C. albicans degrades E-cadherin expressed by oral epithelial cells in vitro; (ii) to compare the abilities of strains with different invasive potentials to degrade this protein; and (iii) to investigate fungal virulence factors responsible for E-cadherin degradation. We found that while E-cadherin gene expression was not altered, E-cadherin was proteolytically degraded during the interaction of oral epithelial cells with C. albicans. Moreover, C. albicans-mediated degradation of E-cadherin was completely inhibited in the presence of protease inhibitors. Using a three-dimensional model of the human oral mucosa, we found that E-cadherin was degraded in localized areas of tissue invasion by C. albicans. An invasion-deficient rim101-/rim101- strain was deficient in degradation of E-cadherin, and this finding suggested that proteases may depend on Rim101p for expression. Indeed, reverse transcription-PCR data indicated that expression of the SAP4, SAP5, and SAP6 genes is severely reduced in the rim101-/rim101- mutant. These SAP genes are functional Rim101p targets, because engineered expression of SAP5 in the rim101-/rim101- strain restored E-cadherin degradation and invasion in the mucosal model. Our data support the hypothesis that there is a mechanism by which C. albicans invades mucosal tissues by promoting the proteolytic degradation of E-cadherin in epithelial adherens junctions.

Indexed as

Gene Expression Regulation, FungalAdherens JunctionsAspartic Acid EndopeptidasesCadherinsCandida albicansCandidiasis, OralCell Line, TumorDNA-Binding ProteinsEpithelial CellsFungal ProteinsHumansMicroscopy, ConfocalMicroscopy, Electron, TransmissionMouth MucosaAspartic Acid EndopeptidasesCadherinsDNA-Binding ProteinsFungal ProteinsRIM101 protein, Candida albicansSAP5 protein, Candida albicans

Identifiers

PMID17339363
PMCPMC1865768
OpenAlexW2140865595

What OpenQuestion holds

Textmetadata
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.