Summary of project PR001114

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 PR001114. The data can be accessed directly via it's Project DOI: 10.21228/M8Q39V This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR001114
Project DOI:doi: 10.21228/M8Q39V
Project Title:Regulation of stress signalling by SCD1-derived phosphatidylinositols
Project Type:Targeted lipidomics
Project Summary:Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation, controlled by stearoyl-CoA desaturase (SCD)1, prevents cytotoxic stress but the mechanisms are diffuse. We found that 1,2-dioleoyl-sn-glycero-3-phospho-(1’-myo-inositol) [PI(18:1/18:1)] is a SCD1-derived signaling lipid, which inhibits p38 mitogen-activated protein kinase (MAPK) activation, counteracts UPR, autophagy and apoptosis induction, and maintains cell morphology and proliferation. SCD1 expression and the cellular PI(18:1/18:1) proportion decrease during the onset of cell death, thereby activating stress signaling. This counter-regulation applies to mechanistically diverse death-inducing conditions and occurs in tissues of Scd1-defective mice.
Institute:University of Innsbruck
Department:Michael Popp Institute
Last Name:Koeberle
First Name:Andreas
Address:Mitterweg 24, Innsbruck, Tyrol, 6020, Austria
Email:andreas.koeberle@uibk.ac.at
Phone:+43 512 507 57903
Funding Source:German Research Council (GRK 1715 and KO 4589/4-1), Phospholipid Research Center Heidelberg (AKO-2019-070/2-1 and AKO-2015-037/1-1), University of Jena (DRM/2013-05 and 2.7-05), Free State of Thuringia (41-5507-2016) and Leibniz ScienceCampus InfectoOptics (SAS-2015-HKI-LWC).
Publications:PI(18:1/18:1) is a SCD1-derived lipokine that limits stress signaling. Thürmer M, Gollowitzer A, Pein H, Neukirch K, Gelmez E, Waltl L, Wielsch N, Winkler R, Löser K, Grander J, Hotze M, Harder S, Döding A, Meßner M, Troisi F, Ardelt M, Schlüter H, Pachmayr J, Gutiérrez-Gutiérrez Ó, Rudolph KL, Thedieck K, Schulze-Späte U, González-Estévez C, Kosan C, Svatoš A, Kwiatkowski M, Koeberle A. Nat Commun. 2022 May 27;13(1):2982. doi: 10.1038/s41467-022-30374-9.

Summary of all studies in project PR001114

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
Release
Date
VersionSamplesDownload
(* : Contains raw data)
ST001740 Timecourse of NIH-3T3 cells treated with apoptotic inducers Mus musculus University of Innsbruck MS 2021-04-20 1 150 Uploaded data (23.4M)*
ST001741 Phospholipid profiling of Scd1-defective mice Mus musculus University of Innsbruck MS 2021-04-20 1 88 Uploaded data (2.9M)*
ST001751 Free fatty acid analysis of NIH-3T3 cells treated with apoptotic inducers Mus musculus University of Innsbruck MS 2021-05-01 1 33 Uploaded data (8M)*
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