Summary of Study ST002334

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001497. The data can be accessed directly via it's Project DOI: 10.21228/M8740F This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002334
Study TitlePhospholipase D3 impact on the endolysosomal lipidome
Study SummaryNeurons rely on the endo-lysosomal network for the maintenance of lipid turnover, removal of dysfunctional organelles and the recycling of proteins. These mechanisms appear to go awry in late-onset Alzheimer’s disease (LOAD). Interestingly, GWA-studies identified risk genes for LOAD linked to endocytic transport regulation (BIN1-CD2AP-PICALM-RIN3-SORL1) and lysosomes (PLD3). Phospholipase D3, also known as PLD3, is a single-pass type II membrane protein that is majorly localized to lysosomes, making it one of the few (or only) risk factors that potentially links lysosomal dysfunction directly to LOAD initiation and progression. CRISPR/Cas9 gene editing was used to generate PLD3 knockout SH-SY5Y cells that were subsequently stably rescued with wild-type PLD3 and coding-variants (M6R & V232M). All cell lines were evaluated for morphological and functional alterations of the endolysosomal compartment, including lipid profiling of endolysosomes magnetically isolated from the different cell lines, as previously described (DOI: 10.1016/j.xpro.2020.100122). A prior isolation step has the unique advantage that it provides spatial resolution to the identified dysregulated networks or compositions. We observe a marked accumulation of storage lipids in endolysosomal isolates; chiefly attributed to cholesterol ester (CE) accretion. A significantly lowered monoacylglycerol level and increased phosphatidylinositol level point to an affected transport/sorting (vesicle/tubule formation).
VIB-KU Leuven
DepartmentCenter for Brain & Disease Research
LaboratoryLaboratory for Membrane Trafficking
Last NameVan Acker
First NameZoë
AddressHerestraat 49 - box 602, 3000 Leuven, Belgium
Submit Date2022-10-27
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailLC-MS
Release Date2022-11-25
Release Version1
Zoë Van Acker Zoë Van Acker application/zip

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Project ID:PR001497
Project DOI:doi: 10.21228/M8740F
Project Title:Phospholipase D3 impact on the endolysosomal lipidome
Project Type:Lipidomics level 2 type quantification as defined by the LSI
Project Summary:Lipidomic analysis of isolated endolysosomes phospholipase D3 (PLD3) knockout and rescues with the wild-type, PLD3-M6R and PLD3-V232M sequences.
Institute:VIB-KU Leuven
Department:Center for Brain & Disease Research
Laboratory:Laboratory for Membrane Trafficking
Last Name:Van Acker
First Name:Zoë
Address:Herestraat 49 - box 602, 3000 Leuven, Belgium
Phone:+32 16 32 07 84
Contributors:Lipid analysis was performed at Lipometrix - KU Leuven Lipidomics Core Facility (Leuven, Belgium).