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Proteomic alterations in the context of survival signaling and redox homeostasis linked to de novo fatty acid biosynthesis

ABSTRACT: Cell death programs like apoptosis, necroptosis, and ferroptosis have an oxidative component linked to lipid metabolism that impacts membrane homeostasis. Evidence for cross-talk between these programs is emerging, highlighting the need for overarching regulatory mechanisms. We investigated changes in the proteome of NIH-3T3 fibroblasts upon induction of cytotoxic stress (valinomycin, myrtucommulone A or serum depletion) and SCD1 inhibition (CAY10566) and addressed the potential of oleic acid (18:1), PI(18:1/18:1) and PI(16:0/16:0) to compensate for the decrease in de novo fatty acid biosynthesis. Please note that parts of the data were previously uploaded to project PXD025396 [http://www.ebi.ac.uk/pride/archive/projects/PXD025396] and reanalyzed for the current project (w/o, VAL, MC, CAY, CAY+ PI(18:1/18:1) and CAY + PI(16:0/16:0)).

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Andreas Koeberle

LAB HEAD: Andreas Koeberle

PROVIDER: PXD053866 | Pride | 2025-01-04

REPOSITORIES: pride

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			Action	DRS
	211118_sh_MK_10_18_1_1.raw	Raw
	211118_sh_MK_11_CAY_1.raw	Raw
	211118_sh_MK_12_18_1_PI_CAY_1.raw	Raw
	211118_sh_MK_13_16_0_PI_CAY_1.raw	Raw
	211118_sh_MK_14_DMSO_2.raw	Raw

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