Summary of project PR002659

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002659. The data can be accessed directly via it's Project DOI: 10.21228/M8Z556 This work is supported by NIH grant, U2C- DK119886. See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR002659
Project DOI:doi: 10.21228/M8Z556
Project Title:Lipidomic analysis of lysosome and hela cell lipids from cells lacking ASAH1
Project Summary:Lysosomes play a central role in cellular homeostasis by degrading proteins internalized through endocytosis and autophagy and recycling their components for organelle biogenesis. Lysosomal Storage Disorders (LSDs) represent a diverse group of diseases that disrupt lysosomal degradation, ion transport, and lipid metabolism. Among these, sphingolipidoses involve defects in glycosphingolipid breakdown, with gene products such as GBA1 identified, and others like SMPD1 and ASAH1 proposed, as genetic risk factors for Parkinson’s disease, although the underlying mechanisms remain poorly defined. In this dataset, we profile lipids from wildtype and ASAH1-/- HeLa cells, as well as from lysosomes isolated from these cells using LysoIP. Consistent with the loss of ASAH1 function, we observe elevated ceramide levels in knockout cells.
Institute:Harvard Medical School
Last Name:Harper
First Name:Wade
Address:25 Shattuck St, Boston, MA 02115
Email:wade_harper@hms.harvard.edu
Phone:8573087183

Summary of all studies in project PR002659

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)		 Release
Date		VersionSamplesDownload
(* : Contains raw data)
ST004217 Lipid Alterations in ASAH1-Deficient Cells: Insights into Ceramide Accumulation and Lysosomal Dysfunction Homo sapiens Harvard Medical School MS 2025-10-14 1 54 Uploaded data (3.4G)*
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