Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA167363 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptomic profiling of HeLa cells infected with Shigella flexneri
| PRJNA305266 | ENA
Project description:We evaluated the transcriptome changes induced by infection of Hela 229 cells with Shigella flexneri. The sample set consists of a control (mock), total population of infected sample and infected sample sorted into Shigella positive and Shigella negative population.
2017-04-04 | GSE75746 | GEO
Project description:HeLa cells AGO2-IP sRNA reads infected and non-infected with Shigella
| PRJNA1277136 | ENA
Project description:Host cells contest invasion by intracellular bacterial pathogens with multiple strategies that recognise and / or damage the bacterial surface. To identify novel host defence factors targeted to intracellular bacteria, we developed a versatile proximity biotinylation approach coupled to quantitative mass spectrometry that maps the host-bacterial interface during infection. Using this method, we discovered that intracellular Shigella and Salmonella become targeted by UFM1-protein ligase 1 (UFL1), an E3 ligase that catalyses the covalent attachment of Ubiquitin-fold modifier 1 (UFM1) to target substrates in a process called UFMylation. We show that Shigella antagonises UFMylation in a dual manner: first, using its lipopolysaccharide (LPS) to shield from UFL1 recruitment; second, preventing UFM1 decoration by the bacterial effector IpaH9.8. Absence of UFMylation leads to an increase of bacterial burden in both human cells and zebrafish larvae, suggesting that UFMylation is a highly conserved antibacterial pathway. Contrary to canonical ubiquitylation, the protective role of UFMylation is independent of autophagy. Here, we used an proteomics-based approach to host effector binding to Shigella in human infected cells. This allowed to confirm UFM1 recruitment to Shigella surface and to identify host effector binding to Shigella in a UFM1-dependent matter. This result reveals potential UFM1 protein substrates on the surface of Shigella in infetec human cells. To do so, we performed siRNA knockdown against UFM1 in HeLa cells prior to infection with the hyperinvasive Shigella flexneri afaI strain considered as the wild-type strain. Alternatively, HeLa cells were infected with S. flexneri ΔrfaCΔipaH9.8 considered as mutant. There were four biological groups with each four replicates: HeLa cells with siUFM1 with wild-type S. flexneri, HeLa cells with non-targeting siRNA with wild-type S. flexneri, siUFM1 with Shigella mutant and non-targeting siRNA with Shigella mutant.
2026-08-17 | PXD075006 | Pride
Project description:Question Addressed: What is the host response (specifically apoptosis pathways) to Shigella infection and what is the contribution of MxiE to the host response? The arrays are apoptosis Exon hit arrays, thus splice variation can be determined. Array data from HeLa cells that remained Uninfected or were infected with wildtype S. flexneri serotype 2a strain 2457T or an isogenic mixE mutant. These groupings are further divided such that Uninfected or Infected cells remained untreated or were treated with the apopotosis inducer staurosporine (STS). The design of the experiment was a time course and samples were harvested at the indicated time points (hr). All hybridizations were conducted against a common reference sample that was made from pooled samples of normal uninfected healthy HeLa cells. Infection: HeLa cells were infected with wt Shigella (wt), mxiE mutant (mixE) or were left uninfected (uninfected) Compound Based Treatment: Cultures were treated with Staurosporin (STS) or were left untreated (untreated) Infection time: Cells were harvested at the indicated time after treatment
2013-05-21 | GSE38086 | GEO
Project description:Question Addressed: What is the host response (specifically apoptosis pathways) to Shigella infection and what is the contribution of MxiE to the host response? The arrays are apoptosis Exon hit arrays, thus splice variation can be determined. Array data from HeLa cells that remained Uninfected or were infected with wildtype S. flexneri serotype 2a strain 2457T or an isogenic mixE mutant. These groupings are further divided such that Uninfected or Infected cells remained untreated or were treated with the apopotosis inducer staurosporine (STS). The design of the experiment was a time course and samples were harvested at the indicated time points (hr). All hybridizations were conducted against a common reference sample that was made from pooled samples of normal uninfected healthy HeLa cells. Infection: HeLa cells were infected with wt Shigella (wt), mxiE mutant (mixE) or were left uninfected (uninfected) Compound Based Treatment: Cultures were treated with Staurosporin (STS) or were left untreated (untreated) Infection time: Cells were harvested at the indicated time after treatment 20 Samples
2013-05-21 | E-GEOD-38086 | biostudies-arrayexpress
Project description:Brucella melitensis-infected HeLa cells gene expression
| PRJNA112203 | ENA
Project description:To discover novel factors that modulate S. flexneri infection, we developed a proteomic-based approach based on the biotin ligation enzyme APEX2. To target the host-Shigella interface, we coated bacteria in vitro prior to infection using anti-GFP nanobody-expressing shigella and recombinant GFP-APEX2. Upon infection in HeLa cells, biotinylated proteins from both host and pathogen were enriched by streptavidin pulldown and identified by mass spectrometry. Here, we analyzed two biological groups where cells were infected with either wild-type Shigella flexneri (S. flexneri) or delta-mixE Shigella flexneri mutant. In each group, four petri dishes were infected to generate four replicates.
2026-08-17 | PXD063609 | Pride
Project description:HeLa/16E6 Cells (Wild-type E2-infected vs. Mock-infected)
| PRJNA104201 | ENA