Evidence map›Paper›PMID 29317695›Full record

ArticleScientific reports2018

Alterations in the properties of the cell membrane due to glycosphingolipid accumulation in a model of Gaucher disease.

Gyula Batta, Lilla Soltész, Tamás Kovács, Tamás Bozó, Zoltán Mészár, Miklós Kellermayer, János Szöllősi, Peter Nagy

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
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  7. Hypoxia Modulates Membrane Mechanics in Pancreatic Cancer.The Journal of membrane biology · 2025
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  18. Inhibition of the HFrontiers in immunology · 2024
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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

8 authors at 2 institutions in 1 country.

Gyula BattaDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Lilla SoltészDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamás KovácsDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamás BozóDepartment of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.
Zoltán MészárDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Miklós KellermayerDepartment of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0002-5553-6553
János SzöllősiDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Peter NagyDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. nagyp@med.unideb.hu.ORCID http://orcid.org/0000-0002-7466-805X
University of Debrecen · HUSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gaucher disease is a lysosomal storage disease characterized by the malfunction of glucocerebrosidase resulting in the accumulation of glucosylceramide and other sphingolipids in certain cells. Although the disease symptoms are usually attributed to the storage of undigested substrate in lysosomes, here we show that glycosphingolipids accumulating in the plasma membrane cause profound changes in the properties of the membrane. The fluidity of the sphingolipid-enriched membrane decreased accompanied by the enlargement of raft-like ordered membrane domains. The mobility of non-raft proteins and lipids was severely restricted, while raft-resident components were only mildly affected. The rate of endocytosis of transferrin receptor, a non-raft protein, was significantly retarded in Gaucher cells, while the endocytosis of the raft-associated GM1 ganglioside was unaffected. Interferon-γ-induced STAT1 phosphorylation was also significantly inhibited in Gaucher cells. Atomic force microscopy revealed that sphingolipid accumulation was associated with a more compliant membrane capable of producing an increased number of nanotubes. The results imply that glycosphingolipid accumulation in the plasma membrane has significant effects on membrane properties, which may be important in the pathogenesis of Gaucher disease.

Indexed as

Cell MembraneCells, CulturedEndocytosisFluorescent Antibody TechniqueGaucher DiseaseGlucosylceramidaseGlycosphingolipidsHumansMacrophagesMembrane MicrodomainsMicroscopy, Atomic ForceMutationSignal TransductionSphingolipidsSTAT Transcription FactorsTransferrinGlucosylceramidaseGlycosphingolipidsSphingolipidsSTAT Transcription FactorsTransferrin

Identifiers

PMID29317695
PMCPMC5760709
OpenAlexW2782382794

What OpenQuestion holds

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LicenceCC BY
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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.