Evidence map›Paper›PMID 28134274›Full record

ArticleScientific reports2017

A novel approach to analyze lysosomal dysfunctions through subcellular proteomics and lipidomics: the case of NPC1 deficiency.

Arun Kumar Tharkeshwar, Jesse Trekker, Wendy Vermeire, Jarne Pauwels, Ragna Sannerud, David A Priestman, Danielle Te Vruchte, Katlijn Vints, Pieter Baatsen, Jean-Paul Decuypere and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Lysosome Enrichment Using Superparamagnetic Iron Oxide Nanoparticles (SPIONs).Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  14. International journal of molecular sciences · 2024
    Article
  15. Regulation of cellular and systemic sphingolipid homeostasis.Nature reviews. Molecular cell biology · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. The expanding organelle lipidomes: current knowledge and challenges.Cellular and molecular life sciences : CMLS · 2023
    Review

15 more citing papers are in PubMed but not listed here.

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

19 authors at 8 institutions in 3 countries.

Arun Kumar TharkeshwarLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
Jesse TrekkerDepartment of Life Science Technology, imec, Leuven, Belgium.
Wendy VermeireLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
Jarne PauwelsVIB Medical Biotechnology Center &Department of Biochemistry, UGent, Ghent, Belgium.
Ragna SannerudLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
David A PriestmanDepartment of Pharmacology, University of Oxford, Oxford, United Kingdom.
Danielle Te VruchteDepartment of Pharmacology, University of Oxford, Oxford, United Kingdom.
Katlijn VintsVIB Bio-imaging core VIB Center for Brain &Disease Research, Leuven, Belgium.
Pieter BaatsenVIB Bio-imaging core VIB Center for Brain &Disease Research, Leuven, Belgium.
Jean-Paul DecuypereLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
Huiqi LuLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
Shaun MartinLaboratory of Cellular Transport Systems, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
Peter VangheluweLaboratory of Cellular Transport Systems, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.
Johannes V SwinnenLaboratory of Lipid Metabolism and Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Liesbet LagaeDepartment of Life Science Technology, imec, Leuven, Belgium.
Francis ImpensVIB Medical Biotechnology Center &Department of Biochemistry, UGent, Ghent, Belgium.
Frances M PlattDepartment of Pharmacology, University of Oxford, Oxford, United Kingdom.
Kris GevaertVIB Medical Biotechnology Center &Department of Biochemistry, UGent, Ghent, Belgium.
Wim AnnaertLaboratory for Membrane Trafficking, VIB Center for Brain &Disease Research, KU Leuven, Department of Neurosciences, Leuven, Belgium.
VIB-KU Leuven Center for Brain & Disease Research · BEUniversity of Oxford · GBVIB-UGent Center for Medical Biotechnology · BEIMEC · BEKU Leuven · BELaboratoire de physique des Solides · FRTransport & Mobility Leuven (Belgium) · BEVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Superparamagnetic iron oxide nanoparticles (SPIONs) have mainly been used as cellular carriers for genes and therapeutic products, while their use in subcellular organelle isolation remains underexploited. We engineered SPIONs targeting distinct subcellular compartments. Dimercaptosuccinic acid-coated SPIONs are internalized and accumulate in late endosomes/lysosomes, while aminolipid-SPIONs reside at the plasma membrane. These features allowed us to establish standardized magnetic isolation procedures for these membrane compartments with a yield and purity permitting proteomic and lipidomic profiling. We validated our approach by comparing the biomolecular compositions of lysosomes and plasma membranes isolated from wild-type and Niemann-Pick disease type C1 (NPC1) deficient cells. While the accumulation of cholesterol and glycosphingolipids is seen as a primary hallmark of NPC1 deficiency, our lipidomics analysis revealed the buildup of several species of glycerophospholipids and other storage lipids in selectively late endosomes/lysosomes of NPC1-KO cells. While the plasma membrane proteome remained largely invariable, we observed pronounced alterations in several proteins linked to autophagy and lysosomal catabolism reflecting vesicular transport obstruction and defective lysosomal turnover resulting from NPC1 deficiency. Thus the use of SPIONs provides a major advancement in fingerprinting subcellular compartments, with an increased potential to identify disease-related alterations in their biomolecular compositions.

Indexed as

Lipid MetabolismProteomicsAutophagosomesCarrier ProteinsCell MembraneDextransEndosomesGene Knockout TechniquesHeLa CellsHumansIntracellular Signaling Peptides and ProteinsLysosomesMagnetite NanoparticlesMembrane GlycoproteinsNanoparticlesNiemann-Pick C1 ProteinCarrier ProteinsDextransferumoxidesIntracellular Signaling Peptides and ProteinsMagnetite NanoparticlesMembrane GlycoproteinsNiemann-Pick C1 ProteinNPC1 protein, humanProteomeSterols

Identifiers

PMID28134274
PMCPMC5278418
OpenAlexW2581510101

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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.