Summary of Study ST001740
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
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.
| Study ID | ST001740 |
| Study Title | Timecourse of NIH-3T3 cells treated with apoptotic inducers |
| Study Type | Targeted lipidomics |
| Study Summary | Time-dependent changes of phosphatidylinositol profiles in mouse NIH-3T3 fibroblasts treated with mechanistically diverse apoptotic inducers. |
| Institute | University of Innsbruck |
| Department | Michael Popp Institute |
| Last Name | Koeberle |
| First Name | Andreas |
| Address | Mitterweg 24, Innsbruck, Tyrol, 6020, Austria |
| andreas.koeberle@uibk.ac.at | |
| Phone | +43 512 507 57903 |
| Submit Date | 2021-04-01 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | wiff |
| Analysis Type Detail | LC-MS |
| Release Date | 2021-04-20 |
| Release Version | 1 |
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Project:
| 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. |
