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Stearic acid blunts growth-factor signaling via oleoylation of GNAI proteins

ABSTRACT: The aim of the MS analysis is to identify fatty acids modifying Cys3 of GNAI3. Detailed description in the manuscript Nuskova et al. submitted to NatComms.

INSTRUMENT(S): ultraflex

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Hana Nuskova

LAB HEAD: Aurelio A. Teleman

PROVIDER: PXD021517 | Pride | 2021-07-22

REPOSITORIES: Pride

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Stearic acid blunts growth-factor signaling via oleoylation of GNAI proteins.

Nůsková Hana H Serebryakova Marina V MV Ferrer-Caelles Anna A Sachsenheimer Timo T Lüchtenborg Christian C Miller Aubry K AK Brügger Britta B Kordyukova Larisa V LV Teleman Aurelio A AA

Nature communications 20210728 1

Covalent attachment of C16:0 to proteins (palmitoylation) regulates protein function. Proteins are also S-acylated by other fatty acids including C18:0. Whether protein acylation with different fatty acids has different functional outcomes is not well studied. We show here that C18:0 (stearate) and C18:1 (oleate) compete with C16:0 to S-acylate Cys3 of GNAI proteins. C18:0 becomes desaturated so that C18:0 and C18:1 both cause S-oleoylation of GNAI. Exposure of cells to C16:0 or C18:0 shifts GNA ...[more]

PMID: 34321466

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Stearic acid blunts growth-factor signaling via oleoylation of GNAI proteins

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2021-08-26 | PXD027064 | Pride

Large scale discovery of coronavirus-host factor protein interaction motifs reveals SARS-CoV-2 disease specific mechanisms and vulnerabilities.

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To identify the nuclear partner(s) of TYRO3 in colon cells using LC-Quadrupole Time-of-Flight Mass Spectrometry.

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The NSP3 protein of SARS-CoV-2 binds fragile X mental retardation proteins to disrupt UBAP2L binding

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2023-12-28 | PXD047232 | Pride

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2023-05-01 | E-MTAB-11819 | biostudies-arrayexpress

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Project description:KDM7A Divergent Transcript (KDM7A-DT) is a stress-induced lncRNAs. In our previous studies, KDM7A-DT showed the most robust cellular phenotype alteration and a significant TP53-dependency upon oxidative and oncogenic stress induction. Since about 50% of human breast cancers have mutant p53 and associated genetic alterations, it is essential to determine what effect a mutant p53 would have on acquired pro-oncogenic functions of KDM7A-DT. In these experiments, we used four antisense LNA Gapmer sequences designed by Exiqon (Vedbaek, Denmark). One of these was a negative control, while the other 3 were designed to target the end of the transcript representing the full-length lncRNA KDM7A-DT (lncRNA; GRCh38/hg38, chr7: 140,178,951-140,179,640). To test the effect of KDM7-DT in the context of mutant p53, we selected the p53-negative luminal BC cells T47D. For each of the LNA gapmers, we utilized 3 technical replicates across two main experimental conditions (normal vs. oxidative stress induced via 30 mins of 0.2 mM H2O2 treatment). Overall, we measured the signals for 47,323 Illumina array probes across 24 individual experiments (4 LNA gapmers * 3 technical replicates * 2 main experimental conditions).

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