Evidence map›Paper›PMID 40076891›Full record

ArticleInternational journal of molecular sciences2025

Lectin-Based Substrate Detection in Fabry Disease Using the Gb3-Binding Lectins StxB and LecA.

Serap Elçin-Guinot, Simon Lagies, Yoav Avi-Guy, Daniela Neugebauer, Tobias B Huber, Christoph Schell, Bernd Kammerer, Winfried Römer

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Serap Elçin-GuinotFaculty of Biology, University of Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany.
Simon LagiesCore Competence Metabolomics, Hilde-Mangold-Haus, University of Freiburg, Habsburgerstraße 19, 79104 Freiburg, Germany.ORCID 0000-0002-5245-1781
Yoav Avi-GuyFaculty of Biology, University of Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany.ORCID 0009-0002-2020-4193
Daniela NeugebauerFaculty of Biology, University of Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany.ORCID 0009-0000-6209-3386
Tobias B HuberIII. Department of Medicine, University Medical Center Hamburg-Eppendorf (UKE), Martinistraße 52, 20246 Hamburg, Germany.
Christoph SchellFaculty of Medicine, Institute for Surgical Pathology Medical Center, University of Freiburg, Breisacher Str. 115A, 70106 Freiburg, Germany.
Bernd KammererBIOSS, Centre for Biological Signaling Studies, University of Freiburg, Schänzlestraße 18, 79104 Freiburg, Germany.
Winfried RömerFaculty of Biology, University of Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany.ORCID 0000-0002-2847-246X

Funding

Deutsche Forschungsgemeinschaft BIOSS - EXC 294Deutsche Forschungsgemeinschaft CIBSS - EXC-2189 - project-ID 390939984Deutsche Forschungsgemeinschaft Heisenberg program (project-ID 501370692)Deutsche Forschungsgemeinschaft Major Research Instrumentation (project-ID 438033605)Deutsche Forschungsgemeinschaft RTG 2202 'Transport across and into membranes' (project-ID 278002225)Deutsche Forschungsgemeinschaft SFB1453 (project-ID 431984000)Deutsche Forschungsgemeinschaft SFB1453 (project P19)Ministry of Science, Research and the Arts of the State of Baden-Württemberg Az: 33-7532.20
6 · The paper itself

Abstract

Fabry disease, the second most common lysosomal storage disorder, is caused by a deficiency of α-galactosidase A (α-Gal A), which leads to an accumulation of glycosphingolipids (GSL), mainly globotriaosylceramide (also known as Gb3). This aberrant GSL metabolism subsequently causes cellular dysfunction; however, the underlying cellular and molecular mechanisms are still unknown. There is growing evidence that damage to organelles, including lysosomes, mitochondria, and plasma membranes, is associated with substrate accumulation. Current methods for the detection of Gb3 are based on anti-Gb3 antibodies, the specificity and sensitivity of which are problematic for glycan detection. This study presents a robust method using lectins, specifically the B-subunit of Shiga toxin (StxB) from

Indexed as

Fabry DiseaseLectinsShiga ToxinTrihexosylceramidesalpha-GalactosidaseFibroblastsGlycosphingolipidsHumansSphingolipidsalpha-GalactosidaseglobotriaosylceramideGlycosphingolipidsLectinsShiga ToxinSphingolipidsTrihexosylceramidesanti-Gb3 antibodyGb3GLA-knockout human podocytesglycosphingolipidsLecAlectinslyso-Gb3lysosomal storage disorderpatient-derived Fabry fibroblastsStxB

Identifiers

PMID40076891
PMCPMC11900420

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.