Proteomics

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Proteomics-based identification of ISG15 modification sites in vivo upon Coxsackie virus infection

ABSTRACT: ISG15 is an interferon-stimulated, ubiquitin-like protein, with anti-viral activity against several clinically relevant viruses. However, its precise mechanism of action during viral infection remains elusive. Upon infection, ISG15 conjugates to protein substrates in covalent manner. We previously found that ISG15 restricts Coxsackie virus (CV) infection both in vitro and in vivo. Here, we endeavored to map the in vivo ISGylome following CV infection to mechanistically elucidate the function of ISG15 in host defense. To do so we combined a genetic approach employing a murine model of deregulated ISGylation with quantitative proteomics of immune-enriched endogenous ISG15 modification sites. In addition, we also quantified protein level changes in the host proteome following infection.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Coxsackievirus Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Fabien Thery  

LAB HEAD: Francis Impens

PROVIDER: PXD032078 | Pride | 2024-05-23

REPOSITORIES: pride

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Dataset's files

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B003790_Ap_CMB-220_FRIMP_GlyGlyIP_Belinglab_CVB3_KO_m42rerun.raw Raw
B003792_Ap_CMB-220_FRIMP_GlyGlyIP_Belinglab_DMEM_WT_m29.raw Raw
B003794_Ap_CMB-220_FRIMP_GlyGlyIP_Belinglab_CVB3_Ci_m46.raw Raw
B003796_Ap_CMB-220_FRIMP_GlyGlyIP_Belinglab_DMEM_KO_m23.raw Raw
B003798_Ap_CMB-220_FRIMP_GlyGlyIP_Belinglab_CVB3_WT_m50.raw Raw
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Publications

<h4>Aims</h4>Virus infection triggers inflammation and, may impose nutrient shortage to the heart. Supported by type I interferon (IFN) signalling, cardiomyocytes counteract infection by various effector processes, with the IFN-stimulated gene of 15 kDa (ISG15) system being intensively regulated and protein modification with ISG15 protecting mice Coxsackievirus B3 (CVB3) infection. The underlying molecular aspects how the ISG15 system affects the functional properties of respective protein subst  ...[more]

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