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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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			Action	DRS
	181121AnalysisParameter.xml	Xml
	181121GNAI3endogenousacylation.zip	Other
	181121MascothomeGNAI3-GFPms1.mht	Other
	181121MascothomeGNAI3-GFPms2.mht	Other
	19030113C18_0.zip	Other

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Publications

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

Project description:The aim of the MS analysis is to identify fatty acids modifying Cys3 of GNAI3 in cells exposed to high C16:0 or C18:0 concentrations. Detailed description in the manuscript Nuskova et al. submitted to NatComms.

2021-08-26 | PXD027064 | Pride

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

Project description:Coronaviruses constitute a constant threat as documented by the recent emergence of SARS-CoV-2 that has caused more than 2,5 million deaths worldwide. Despite this our understanding of coronaviruses and how they interact with their host is very limited. Here we describe a novel phage display library for the discovery of viral short linear interaction motifs (SLiMs) from RNA viruses that mediate binding to human host factors. We utilize this library to uncover the unique patterns of viral SLiMs mediating SARS-CoV-2 - host factor interactions. This established a specific interaction between the human G3BP1/2 proteins and an xFG peptide motif in the viral nucleocapside (N) protein that when disrupted reduce viral replication and infection. We show that the N protein through this xFG motif modulates the G3BP1/2 host interactome by competing with numerous cellular xFG containing proteins and inhibits G3BP1/2 mediated stress granule formation. Collectively our work outlines a strategy for system-wide understanding of viral-host factor interactions that provides both mechanistic insight and pinpoints therapeutically relevant interactions for development of novel antiviral strategies.

2021-10-29 | PXD025410 | Pride

mRNA binding - Insights into RNA biology from an atlas of mammalian mRNA-binding proteins

Project description:RNA-binding proteins (RBPs) determine RNA fate from synthesis to decay. Employing two complementary protocols for covalent UV crosslinking of RBPs to RNA, we describe a systematic, unbiased, and comprehensive approach, termed "interactome capture," to define the mRNA interactome of proliferating human HeLa cells. We identify 860 proteins that qualify as RBPs by biochemical and statistical criteria, adding more than 300 RBPs to those previously known and shedding light on RBPs in disease, RNA-binding enzymes of intermediary metabolism, RNA-binding kinases, and RNA-binding architectures. Unexpectedly, we find that many proteins of the HeLa mRNA interactome are highly intrinsically disordered and enriched in short repetitive amino acid motifs. Interactome capture is broadly applicable to study mRNA interactome composition and dynamics in varied biological settings.

2015-09-11 | PXD002880 | Pride

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

Project description:Colorectal cancer (CRC) is one of the most common death-related cancers worldwide. Aberrant expression of oncogenes is regarded as a predominant factor in CRC development. In our study, we found that TYRO3 intracellular domain nuclear translocation promotes CRC cell proliferation, metastasis, and tumor progression. To identify downstream effector that transmits the cellular functions of nuclear TYRO3, we performed nuclear TYRO3 co-immunoprecipitation.

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

Project description:Viruses interact with numerous host factors to facilitate viral replication and to dampen antiviral defense mechanisms. We currently have a limited mechanistic understanding of how SARS-CoV-2 binds host factors and the functional role of these interactions. Here, we uncover a novel interaction between the viral NSP3 protein and the fragile X mental retardation proteins (FMRPs: FMR1 and FXR1-2). SARS-CoV-2 NSP3 mutant viruses preventing FMRP binding have slightly attenuated replication in vitro and reduced levels of viral antigen in lungs during early stages of infection. We show that a unique peptide motif in NSP3 binds directly to the two central KH domains of FMRPs and that this interaction is disrupted by the I304N mutation found in a patient with fragile X syndrome. NSP3 binding to FMRPs disrupts their interaction with the stress granule component UBAP2L through direct competition with a peptide motif in UBAP2L to prevent FMRP incorporation into stress granules. Collectively, our results provide novel insight into how SARS-CoV-2 hijacks host cell proteins and provides molecular insight to the possible underlying molecular defects in fragile X syndrome.

2023-12-28 | PXD047232 | Pride

Illumina Microarray of MRC5 cell with or without KDM7A-DT overexpression

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. To investigate the functional roles of KDM7A-DT, we first performed overexpression experiments using fibroblasts. We found that MRC5 cells overexpressing KDM7A-DT escaped cell cycle proliferation and long-term survival ability and were associated with a distinct stress-related morphology (enlarged and flattened cells) compared to cells expressing just the vehicle control. To examine the effects of KDM7A-DT overexpression on the transcriptome, we performed a differential expression gene (DEG) analysis comparing a group of four independent biological replicates of MRC5 overexpressing KDM7A-DT to a group of samples from control cells.

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