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Identifying changes in host responses to Yersinia infection in the presence or absence of YopM virulence factor

ABSTRACT: Transcriptional profiling of total splenic RNA isolated from Yersinia pestis infected mice, comparing samples from YopM-competent parental strain (D27) infected mice to infected mice with YopM-deficient strain (M') at 1hr and 16hr post infection 4 groups. Biological replicates per group: n=3. One replicate per array.

ORGANISM(S): Mus musculus

SUBMITTER: June Brickey

PROVIDER: E-GEOD-41564 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identifying changes in host responses to Yersinia infection in the presence or absence of YopM virulence factor

Project description:Transcriptional profiling of total splenic RNA isolated from Yersinia pestis infected mice, comparing samples from YopM-competent parental strain (D27) infected mice to infected mice with YopM-deficient strain (M') at 1hr and 16hr post infection

2012-10-16 | GSE41564 | GEO

ARIH2 is a novel Vif-dependent regulator of CUL5-mediated APOBEC3G degradation in HIV infection

Project description:Discovery of novel host-virus interactions leads to a better understanding of mechanisms underlying infection and points to potential therapeutic targets at the interface between virus and host proteins. Recently, global, virus-host interaction networks have been mapped using affinity purification-mass spectrometry (AP-MS) approaches, but these studies do not provide information about dynamic remodeling of host complexes during infection. Here, we describe a novel quantitative proteomics approach in the context of HIV infection to unravel dynamics of the Cullin RING E3 ligase 5 (CRL5) complex, which is hijacked by HIV Vif to degrade the viral restriction factor of the APOBEC3 family. Generating a dynamic and quantitative interaction network of CRL5 under various infection conditions, we identify the E3 ligase ARIH2 as novel regulator of APOBEC3G degradation, which is essential for HIV infectivity in primary CD4+ T-cells. ARIH2 acts in a “tag-team” mechanism that accelerates ubiquitin chain formation on APOBEC3G through CUL5Vif/CBFß by priming the substrate with mono-ubiquitination. Finally, our data suggest a general role for ARIH2 in CRL5 substrate ubiquitination in host cells.

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2008-04-15 | E-GEOD-11076 | biostudies-arrayexpress

Myeloid Derived Suppressor Cells and Cancer

Project description:Transcriptional profiling of FACS-sorted and splenic control mouse cells, comparing splenic cells from FVBneuN vs Neu+ expressing FVBneuN mice with Gr1+ CD11b+ sorted tumor-infiltrating mononuclear or splenic myeloid-derived suppressor cells 4 groups or conditions. Biological replicates: 2 or 3 per condition. One replicate array per sample. manuscript: van Deventer, H, J Burgents, QP Wu, R Woodford, WJ Brickey, I Allen, E McElvania-Tekippe, J Serody, and J Ting. (2010) The inflammasome component Nlrp3 impairs antitumor vaccine by enhancing the accumulation of tumor-associated myeloid-derived suppressor cells. Cancer Research. variable: cell type: splenic cells from normal FVB-neuN mice, splenic cells from Neu+ tumor-bearing FVB-neuN mice, Gr1+ CD11b+ sorted cells from tumor, Gr1+ CD11b+ sorted cells from spleen repear: biological replicate: #1, #2, #3

2010-12-29 | E-GEOD-26289 | biostudies-arrayexpress

ChIP-seq of primary human macrophages uninfected or infected with Yersinia enterocolitica strains

Project description:Pathogenic bacteria Yersinia enterocolitica injects virulence plasmid-encoded effectors through the type three secretion system into macrophages to modulate gene expression. At this point it is not known whether epigenetic modifications play a role in Yersinia regulation of gene expression. To answer this question primary human macrophages were infected with mock, WAC (virulence plasmid-cured strain) or WA314 (wild type) and samples were subjected to ChIP-seq for H3K4me3, H3K4me1, H3K27ac and H3K27me3. The effect of effector proteins YopM and YopP on histone modifications in macrophages was analyzed using a wild type strain lacking either YopM or YopP and subsequent ChIP-seq analysis.

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Project description:Gut microbiota of pups born to yopM-infected mothers

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Differential expression of miRNA in stretched rat alveolar epithelial cells

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