Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phosphoproteomics analysis of CHIKV-infected RAW264.7 macrophages

ABSTRACT: To characterize host cellular responses associated with CHIKV infection, we performed mass spectrometry-based phosphoproteomic profiling of CHIKV-infected RAW264.7 macrophages. Analysis of enriched phosphoproteins identified 2,096 altered proteins compared with mock-infected controls. These findings suggest that host protein responses during CHIKV infection, may provide insights for the development of future antiviral strategies.

ORGANISM(S): Mus Musculus

SUBMITTER: Kobporn Boonnak

PROVIDER: PXD076345 | iProX | Mon Mar 30 00:00:00 BST 2026

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus

Project description:RAW264.7 macrophages infected with MNV-1 and mock infected gene expression measured by microarray. To be published in Waugh, E. Chen, A. Baird, M. Fleming, S. Brown, C.M. and V K. Ward (2014) Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus. Virus Genes

2013-12-22 | GSE50093 | GEO

Characterization of the chemokine response of RAW264.7 cells to infection by murine norovirus

2013-12-22 | E-GEOD-50093 | biostudies-arrayexpress

Gene expression in Src-/- RAW264.7 cells infected with VSV and HSV-1

Project description:The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

2016-07-01 | E-GEOD-81675 | biostudies-arrayexpress

Toxoplasma RH and Mock Infection of macrophages

Project description:Infection of RAW264.7 cells with RHΔku80 parasites or mock-infection for 24 hours To measure changes in gene expression induced in macropahges upon Toxoplasma infection, we infected RAW 264.7 macrophages in cell culture with RHΔku80 parasites or syringe-lysed human foreskin fibroblast monolayers (mock-infected). RNA was harvested 24 hours post infection.

2014-02-25 | GSE55298 | GEO

Gene expression in Tao3−/− RAW264.7 cells infected with VSV and HSV-1

Project description:The purpose of this study was to determine what are the effects of TAO3 deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Tao3−/− RAW264.7 cells were infected with Vesicular Stomatitis Virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed.

2023-02-01 | GSE97704 | GEO

Gene expression in Src-/- RAW264.7 cells infected with VSV and HSV-1

2016-07-01 | GSE81675 | GEO

Toxoplasma RH and Mock Infection of macrophages

Project description:Infection of RAW264.7 cells with RH?ku80 parasites or mock-infection for 24 hours To measure changes in gene expression induced in macropahges upon Toxoplasma infection, we infected RAW 264.7 macrophages in cell culture with RH?ku80 parasites or syringe-lysed human foreskin fibroblast monolayers (mock-infected). RNA was harvested 24 hours post infection. Cells were infected with Toxoplasma or mock-infected in vitro, in duplicate

2014-02-25 | E-GEOD-55298 | biostudies-arrayexpress

Expression data from RAW264.7 murine macrophages infected with Toxoplasma gondii and subsequently stimulated with interferon-gamma

Project description:Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe). We used Affymetrix microarrays to analyze host cell transcription after Toxoplasma infection and interferon-gamma stimulation. RAW264.7 murine macrophages were left uninfected or infected with type I (RH), type I ?rop16 (RH ?rop16), type II (Pru), type II ?gra15 (Pru ?gra15), or type II (CEP) parasites at an MOI ~5 for 18 hours and subsequently stimulated with murine IFN-? for six hours. Plaque assays were done to assess parasite viability. Total RNA was isolated and hybridized to Affymetrix Mouse 430A 2.0 gene chips.

2013-02-19 | E-GEOD-34913 | biostudies-arrayexpress

Genome-wide maps of gene transcription levels in RAW264.7 infected with CdhM-related Mycobacterium tuberculosis H37Ra strain.

Project description:We report the application of RNA-seq technology for high-throughput profiling of gene transcription in RAW264.7 infected with Mycobacterium tuberculosis H37Ra. By obtaining over six billion bases of sequence from mRNA, we generated genome-wide gene transcription maps of RAW264.7 infected with CdhM-related Mycobacterium tuberculosis H37Ra. We find that numerous genes involved in ER stress are significantly affected by CdhM. This finding indicates that CdhM may induce ER stress during Mtb infection of host cells.

2022-02-24 | GSE196961 | GEO

Interferon Lambda Alleles Predict Innate Antiviral Immune Responses and Hepatitis C Virus Permissiveness.

Project description:Hepatitis C virus (HCV) infection can result in viral chronicity or clearance. Although host genetics and particularly genetic variation in the interferon lambda (IFNL) locus are associated with spontaneous HCV clearance and treatment success, the mechanisms guiding these clinical outcomes remain unknown. Using a laser capture microdissection-driven unbiased systems virology approach, we isolated and transcriptionally profiled HCV-infected and adjacent primary human hepatocytes (PHH) approaching single cell resolution. An innate antiviral immune signature dominated the transcriptional response, but differed in magnitude and diversity between HCV-infected and adjacent cells. Molecular signatures associated with more effective antiviral control were determined by comparing donors with high and low infection frequencies. Cells from donors with clinically unfavorable IFNL genotypes were infected at a greater frequency and exhibited dampened antiviral and cell death responses. These data suggest that early virus-host interactions, particularly host genetics and induction of innate immunity, critically determine the outcome of HCV infection. Cell populations of primary human hepatocytes were collected via laser capture microdissection, their transcriptomes were amplified and analyzed via whole Illumina genome microarray. Three populations were collected: virus infected cells, cells adjacent to infected cells (“adjacent”) and mock infected cells. Cells from multiple donors were employed to address host genetic variability on our observed phenotypes. Nine different donors were assessed on 1-day post infection and three donors were assessed 3 days post infection and and four donors were assessed on 7 days post infection. For each cell population (virus infected, adjacent or mock), four biological replicate arrays were performed. In total, we analyzed 186 microarrays

2014-02-12 | E-GEOD-54648 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data