Virus Expression Database

GSE19772

Expression Data From HCMV-Infected Human Monocytes 48 Hours Post-Infection: Role of PI(3)K

Submitted by Andrew D Yurochko (LSUHSC-S, USA) on Jan 06 2010

Platform: microarray – [HG_U95Av2] Affymetrix Human Genome U95 Version 2 Array

Pubmed: 20173022

Summary Human cytomegalovirus (HCMV) induces pro-inflammatory monocytes following infection and we have evidence that phosphatidylinositol 3-kinase [PI(3)K] is a key mediator in this activation. To begin to address how this signalling pathway is responsible for the functional changes in infected monocytes, we examined the role this pathway played in the transcriptome of infected monocytes. Global transcriptional profiling using cDNA microarrays revealed a significant number of genes were regulated in a PI(3)K-dependent manner, identifying this pathway as a key cellular control point in the conversion of monocytes to an activated pro-inflammatory state following HCMV infection.

Keywords: Disease state

6 Samples

ID Title Cell Type Timepoint Reported Virus Virus Species Exclusion Reason
GSM493878 Mock-infected monocyte, 48 hr post-infection, biological rep1 monocyte  48 hrs mock Uninfected
GSM493879 Mock-infected monocyte, 48 hr post-infection, biological rep2 monocyte  48 hrs mock Uninfected
GSM493880 HCMV-infected monocyte, 48 hr post-infection, biological rep1 monocyte  48 hrs HCMV Human betaherpesvirus 5
GSM493881 HCMV-infected monocyte, 48 hr post-infection, biological rep2 monocyte  48 hrs HCMV Human betaherpesvirus 5
GSM493882 HCMV-infected/LY-pretreated monocyte, 48 hr post-infection, biological rep1 monocyte  48 hrs HCMV Human betaherpesvirus 5 Extra interventions
PI3K inhibitor
GSM493883 HCMV-infected/LY-pretreated monocyte, 48 hr post-infection, biological rep2 monocyte  48 hrs HCMV Human betaherpesvirus 5 Extra interventions
PI3K inhibitor