Evidence map›Paper›PMID 24828903›Full record

ReviewClinical reviews in allergy & immunology2015

Fucosyltransferase 2: a genetic risk factor for primary sclerosing cholangitis and Crohn's disease--a comprehensive review.

Luca Maroni, Stan F J van de Graaf, Simon D Hohenester, Ronald P J Oude Elferink, Ulrich Beuers

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Association of Fucosyltransferase 2 Gene Variant with Inflammatory Bowel Diseases: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019
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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 2 countries.

Luca MaroniDepartment of Gastroenterology and Hepatology, Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1100 DD, Amsterdam, The Netherlands.
Stan F J van de Graaf
Simon D Hohenester
Ronald P J Oude Elferink
Ulrich Beuers
University of Amsterdam · NLAcademic Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fucosyltransferase 2 (FUT2) mediates the inclusion of fucose in sugar moieties of glycoproteins and glycolipids. ABO blood group antigens and host-microbe interactions are influenced by FUT2 activity. About 20 % of the population has a "non-secretor" status caused by inactivating variants of FUT2 on both alleles. The non-sense mutation G428A and the missense mutation A385T are responsible for the vast majority of the non-secretor status in Caucasians, Africans, and Asians, respectively. Non-secretor individuals do not secrete fucose-positive antigens and lack fucosylation in epithelia. They also appear to be protected against a number of infectious diseases, such as Norovirus and Rotavirus infections. In recent years, genome-wide association studies (GWAS) identified inactivating variants at the FUT2 locus to be associated with primary sclerosing cholangitis (PSC), Crohn's disease (CD), and biochemical markers of biliary damage. These associations are intriguing given the important roles of fucosylated glycans in host-microbe interactions and membrane stability. Non-secretors have a reduced fecal content of Bifidobacteria. The intestinal bacterial composition of CD patients resembles the one of non-secretors, with an increase in Firmicutes and decreases in Proteobacteria and Actinobacteria. Non-secretor individuals lack fucosylated glycans at the surface of biliary epithelium and display a different bacterial composition of bile compared to secretors. Notably, an intact biliary epithelial glycocalix is relevant for a stable 'biliary HCO3 (-) umbrella' to protect against toxic effects of hydrophobic bile salt monomers. Here, the biology of FUT2 will be discussed as well as hypotheses to explain the role of FUT2 in the pathophysiology of PSC and Crohn's disease.

Indexed as

AnimalsCholangitis, SclerosingColitis, UlcerativeCrohn DiseaseFucoseFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansRisk FactorsFucoseFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferase

Identifiers

PMID24828903
OpenAlexW2084671232

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.