Evidence map›Paper›PMID 30291216›Full record

ArticleBioscience reports2018

Inhibition of N-glycosylation by tunicamycin attenuates cell-cell adhesion via impaired desmosome formation in normal human epidermal keratinocytes.

Seon-Pil Jin, Jin Ho Chung

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022
    Review
  10. Article
  11. Lectin-Mediated Bacterial Modulation by the Intestinal NematodeInternational journal of molecular sciences · 2021
    Article
  12. Article
  13. Altered glycosylation in cancer: A promising target for biomarkers and therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  14. Article
  15. 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

2 authors at 1 institution in 1 country.

Seon-Pil JinDepartment of Dermatology, Seoul National University Hospital, Seoul 03080, Republic of Korea.
Jin Ho ChungDepartment of Dermatology, Seoul National University Hospital, Seoul 03080, Republic of Korea jhchung@snu.ac.kr.
Seoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

N-Glycosylation affects protein functions such as location, stability, and susceptibility to proteases. Desmosomes in keratinocytes are essential to maintain epidermal tissue integrity to protect against environmental insults. However, it is not yet known whether N-glycosylation affects desmosomal functions in primary keratinocytes. Tunicamycin is an inhibitor of N-glycosylation that has been a useful tool in glycobiology. Therefore, we investigated the effect of inhibiting N-glycosylation by tunicamycin treatment on desmosomes in primary keratinocytes. In our experiments, cell-cell adhesive strength was reduced in tunicamycin-treated primary keratinocytes. TEM showed that desmosome formation was impaired by tunicamycin. Desmogleins (Dsgs) 1 and 3, which constitute the core structure of desmosomes, were well transported to the cell-cell borders, but the amount decreased and showed an aberrant distribution at the cell borders in tunicamycin-treated keratinocytes. The stability of both desmoglein proteins was also reduced, and they were degraded through both proteasomal and lysosomal pathways, although inhibiting degradation did not restore the cell-cell adhesion. Finally, tunicamycin induced desmosomal instability, enhancing their disassembly. In conclusion, these results indicate that N-glycosylation is critical to the desmosome complex to maintain cell-cell adhesive strength in primary keratinocytes.

Indexed as

Cell AdhesionDesmoglein 1Desmoglein 3DesmosomesEpidermisGlycosylationHumansKeratinocytesMetabolic Networks and PathwaysPrimary Cell CultureTunicamycinDesmoglein 1Desmoglein 3Tunicamycincell adhesiondesmosomeskeratinocytesN-glycosylationtunicamycin

Identifiers

PMID30291216
PMCPMC6259015
OpenAlexW2894920234

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.