Evidence map›Paper›PMID 42271546›Full record

ArticleJournal of inherited metabolic disease2026

Validating a Human Cell Model of Null Galactosylceramidase (GALC) Enzyme Activity That Recapitulates Krabbe Disease.

Rodrigo T Starosta, Nazia Khatoon, Marie S Roberts, Steven Q Le, Grant Austin, Xiaoxia Cui, Gregory Strout, Robert E Schmidt, Xuntian Jiang, Mark S Sands and 1 more

Abstract read
In one paragraph

Article in Journal of inherited metabolic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

11 authors.

Rodrigo T StarostaDepartment of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.
Nazia KhatoonDepartment of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.
Marie S RobertsDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Steven Q LeDepartment of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.
Grant AustinDepartment of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.
Xiaoxia CuiMcDonnell Genomics Institute, Washington University School of Medicine, St. Louis, Missouri, USA.
Gregory StroutWashington University Center for Cellular Imaging, St. Louis, Missouri, USA.
Robert E SchmidtDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.
Xuntian JiangDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Mark S SandsDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Patricia I DicksonDepartment of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, USA.

Funding

Systems-Level Approach to Neuronopathic Lysosomal Storage DisordersRM1NS132962 · NINDS · WASHINGTON UNIVERSITY · PI JONATHAN D COOPER, PATRICIA I DICKSON · 2023 to 2026
$6.3M
NIH HHS 1R38 AI74266NIH HHS 1RM1 NS132962NINDS NIH HHS RM1 NS132962Washington University in St. Louis
6 · The paper itself

Abstract

Krabbe Disease (KD) is a lysosomal leukodystrophy characterized by the production of psychosine in oligodendrocytes, leading to neurodegeneration and ultimately death. The only treatment modality currently available for this disease is hematopoietic stem cell transplantation (HSCT), a procedure with high morbidity, highlighting the need for further therapies to be developed. In this study, we established and characterized GALC knockout MO3.13 cells, a cell line derived from human oligodendrocytes, as a model for KD. Clonal MO3.13 cells with GALC KO were obtained via CRISPR/Cas9-mediated gene editing. GALC activity was measured by a 4-methylumbellyferyl (4-MU)-based assay, and morphology analyses were performed using light microscopy and transmission electron microscopy. Psychosine was measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The GALC KO cells have elevated levels of psychosine and an increased number of autophagosomes, autolysosomes, and cytoplasmic granules on transmission electron microscopy. Glycogen abundance was decreased in GALC KO cells compared to controls. After administration of BMN-S202, a ceramide galactosyltransferase inhibitor, psychosine levels in GALC KO cells were reduced back to WT levels. In conclusion, we demonstrated that the GALC KO MO3.13 cell line recapitulates the KD phenotype and biochemical response to SRT and may be a useful KD model for mechanistic studies and therapeutic development for KD.

Indexed as

GalactosylceramidaseLeukodystrophy, Globoid CellCell LineChromatography, LiquidGene Knockout TechniquesGlycogenHumansOligodendrogliaPsychosineTandem Mass SpectrometryGalactosylceramidaseGlycogenPsychosinegalactosylsphingosinegloboid cell leukodystrophyglycogenKrabbe diseaselysosomal storage disorderMO3.13oligodendrocyte

Identifiers

PMID42271546
PMCPMC13370254

What OpenQuestion holds

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Registered trials

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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.