Dataset Information

Proteome and phosphoproteome profiling of HCT116 colon cancer cells with PP2A subunit PR130 deletion and herpes simplex virus HSV-1 infection

ABSTRACT: Label-free quantitative proteomics and phosphoproteomics experiments were performed to study the impact of PP2A subunit PR130 deletion and herpes simplex virus HSV-1 infection on differential protein expression and phosphorylation changes in HCT116 human colon cancer cells.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Human Alphaherpesvirus 1

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Colon Cancer

SUBMITTER: Jia-Xuan Chen

LAB HEAD: Oliver H. Krämer

PROVIDER: PXD067327 | Pride | 2026-05-16

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20241017_AST1_EXT_CF_1436_1_PR_NON_DIA_60.raw	Raw
	20241017_AST1_EXT_CF_1436_2_PHOS_NON_DIA_60.raw	Raw
	20241017_AST1_EXT_CF_1437_1_PR_NON_DIA_60.raw	Raw
	20241017_AST1_EXT_CF_1437_2_PHOS_NON_DIA_60.raw	Raw
	20241017_AST1_EXT_CF_1438_1_PR_NON_DIA_60.raw	Raw

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Publications

The Host Cell Factor Phosphatase-2A Subunit PR130 Restricts Replication of Herpes Simplex Virus Type-1.

Jungwirth Johannes J Jacob Christoph F CF Nguyen Alexandra A Beyer Mandy M Mieland Andreas O AO Dejung Mario M Chen Jia-Xuan JX Brenner Walburgis W Ehrhardt Christina C Henke Andreas A Krämer Oliver H OH

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20260515

Herpes simplex virus type-1 (HSV-1) affects over 60% of the human population and increasingly develops resistance to antiviral therapies. Efficient HSV-1 replication requires host-derived deoxynucleotide triphosphates and the manipulation of cellular DNA replication and repair. This work positions the protein phosphatase 2A (PP2A) regulatory subunit PR130 (PPP2R3A) as cellular factor that suppresses the replication of laboratory strains and clinical isolates of HSV-1 in epithelial and neuronal c ...[more]

PMID: 42138961

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Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.