Evidence map›Paper›PMID 21104290›Full record

ReviewCellular and molecular life sciences : CMLS2011

Modulation of E-cadherin function and dysfunction by N-glycosylation.

Salomé S Pinho, Raquel Seruca, Fátima Gärtner, Yoshiki Yamaguchi, Jianguo Gu, Naoyuki Taniguchi, Celso A Reis

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
–field-weighted citation impact
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

86 citing papers in PubMed.

  1. Article
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  4. Review
  5. Chemical inhibition of α-mannosidase inFrontiers in parasitology · 2026
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  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Insights into E-Cadherin Impairment inInternational journal of molecular sciences · 2024
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

26 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

7 authors.

Salomé S PinhoInstitute of Molecular Pathology and Immunology University of Porto, Portugal.
Raquel Seruca
Fátima Gärtner
Yoshiki Yamaguchi
Jianguo Gu
Naoyuki Taniguchi
Celso A Reis

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several mechanisms have been proposed to explain the E-cadherin dysfunction in cancer, including genetic and epigenetic alterations. Nevertheless, a significant number of human carcinomas have been seen that show E-cadherin dysfunction that cannot be explained at the genetic/epigenetic level. A substantial body of evidence has appeared recently that supports the view that other mechanisms operating at the post-translational level may also affect E-cadherin function. The present review addresses molecular aspects related to E-cadherin N-glycosylation and evidence is presented showing that the modification of N-linked glycans on E-cadherin can affect the adhesive function of this adhesion molecule. The role of glycosyltransferases involved in the remodeling of N-glycans on E-cadherin, including N-acetylglucosaminyltransferase III (GnT-III), N-acetylglucosaminyltransferase V (GnT-V), and the α1,6 fucosyltransferase (FUT8) enzyme, is also discussed. Finally, this review discusses an alternative functional regulatory mechanism for E-cadherin operating at the post-translational level, N-glycosylation, that may underlie the E-cadherin dysfunction in some carcinomas.

Indexed as

Models, BiologicalCadherinsCarcinomaCell AdhesionGlycosylationGlycosyltransferasesHumansModels, MolecularPolysaccharidesProtein Processing, Post-TranslationalCadherinsGlycosyltransferasesPolysaccharides

Identifiers

PMID21104290
PMCPMC11114786

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.