Evidence map›Paper›PMID 7878011›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Expression of a human alpha-1,3/4-fucosyltransferase in the pit cell lineage of FVB/N mouse stomach results in production of Leb-containing glycoconjugates: a potential transgenic mouse model for studying Helicobacter pylori infection.

P G Falk, L Bry, J Holgersson, J I Gordon

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
12.3field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 133 citations in OpenAlex.

  1. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
    Review
  2. Article
  3. Enhanced Fitness of a Helicobacter pyloriInfection and immunity · 2021
    Article
  4. Toxins · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Host Lewis phenotype-dependent Helicobacter pylori Lewis antigen expression in rhesus monkeys.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2006
    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

4 authors at 1 institution in 1 country.

P G FalkDepartment of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110.
L Bry
J Holgersson
J I Gordon
Washington University in St. Louis · US

Funding

TRANSGENIC AND CHIMERIC-TRANSGENIC MOUSE MODELS FOR GASTRIC EPITHELIUM BIOLOGYP01DK033487 · NIDDK · WASHINGTON UNIVERSITY · PI GORDON, JEFFREY IVAN · 1987 to 2000
$1.1M
MOLECULAR GENETICS OF INTESTINAL DEVELOPMENTR01DK037960 · NIDDK · WASHINGTON UNIVERSITY · PI GORDON, JEFFREY IVAN · 1987 to 1999
–
NIDDK NIH HHS DK33487NIDDK NIH HHS DK37960
6 · The paper itself

Abstract

Helicobacter pylori is a human pathogen associated with the development of gastric and duodenal ulcers and gastric adenocarcinoma. To test the hypothesis that the human Lewis(b) blood group antigen (Le(b)) functions as a receptor for the bacteria's adhesins and mediates its attachment to gastric pit and surface mucous cells, a human alpha-1,3/4-fucosyltransferase was expressed in these cell lineages in FVB/N transgenic mice. The fucosyltransferase directed production of the Leb epitope without any apparent effect on the proliferation and differentiation programs of this lineage. Moreover, clinical isolates of H. pylori bound to these cells in transgenic mice but not in their normal littermates. Binding was blocked by pretreatment of the bacteria with soluble Le(b). This mouse model could be useful for examining the molecular pathogenesis of diseases caused by H. pylori infection. Creating novel pathways for production of specific oligosaccharides in selected cell lineages of transgenic animals represents an approach for examining the role of complex carbohydrates in regulating cellular differentiation and host-microbe interactions.

Indexed as

Lewis Blood Group AntigensAnimalsCarbohydrate SequenceDisease Models, AnimalFucosyltransferasesGastric MucosaGlycoconjugatesHelicobacter InfectionsHelicobacter pyloriHumansIntestinal MucosaMiceMice, TransgenicMolecular Sequence DataTissue Distribution3-galactosyl-N-acetylglucosaminide 4-alpha-L-fucosyltransferaseFucosyltransferasesGlycoconjugatesLewis Blood Group Antigens

Identifiers

PMID7878011
PMCPMC42550
OpenAlexW1991447989

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.