PP2A regulates inflammatory cytokine/chemokine gene expression by dephosphorylating protein kinases at multiple signaling pathways from stimulated cells. In this dataset, Affymetrix mouse Gene ST 2.1 Array was used to assay total RNA extracted from LPS-treated PP2AC knockout BMDM (PP2ACfl/fl;lyM-Cre) and the control BMDM (PP2ACfl/fl)
Myeloid-Specific Gene Deletion of Protein Phosphatase 2A Magnifies MyD88- and TRIF-Dependent Inflammation following Endotoxin Challenge.
Specimen part
View SamplesWe present a novel method of using commercial oligonucleotide expression microarrays for aCGH, enabling DNA copy number measurements and expression profiles to be combined using the same platform. This method yields aCGH data from genomic DNA without complexity reduction at a median resolution of approximately 17,500 base pairs. Due to the well-defined nature of oligonucleotide probes, DNA amplification and deletion can be defined at the level of individual genes and can easily be combined with gene expression data.
Gene-resolution analysis of DNA copy number variation using oligonucleotide expression microarrays.
No sample metadata fields
View SamplesWe analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.
Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer.
Cell line, Time
View SamplesWe report the RNA-Seq data of microglia from CK-p25 mice visual cortex Overall design: Summary of mice and treatments included in this series: CK-p25 mice - in which the expression of the Cdk5 activator p25 is driven by the excitatory neuron-specific CaMKIIa promoter in an inducible manner (CaMKIIa promoter- tTA x TetO- p25+GFP) (Cruz et al., 2003). Following withdrawal of doxycycline from the diet, CK-p25 exhibit progressive neuronal and synaptic loss with cognitive impairment, which is severe by 6 weeks of p25 induction (Cruz et al., 2003). Tau P301S mice, which express high levels of humanized mutant microtubule-associated protein tau and have tau aggregates that are associated with frontotemporal dementia as early as 5 months of age (Yoshiyama et al., 2007). 8 months old P301S mice, at which age they have synaptic and neuronal loss and cognitive deficits. CK = wild type control mice; CK-p25 + No Stim = CK-p25 mice that did not under go any stimulation; CK-p25 +GENUS = Ck-p25 mice that was stimulated with 40 Hz visual stimulation WT = wild type control mice; P301S + No Stim = P301S mice that did not under go any stimulation; P301S +GENUS = P301S mice that was stimulated with 40 Hz visual stimulation
Gamma Entrainment Binds Higher-Order Brain Regions and Offers Neuroprotection.
Specimen part, Subject
View SamplesSeasonal and pandemic influenza is a cause of morbidity and mortality worldwide. Most people infected with influenza virus display mild to moderate disease phenotypes and recover within a few weeks.
Epigenetic and Transcriptomic Regulation of Lung Repair during Recovery from Influenza Infection.
Specimen part
View SamplesTranscriptional changes were analyzed in two colorectal cancer, two pancreatic cancer, and one small cell lung cancer cell line following treatment with the BET inhibitor GSK525762 and/or the MEK inhibitor trametinib using Affymetrix Human Genome U133 Plus 2.0 Arrays.
MEK inhibitors overcome resistance to BET inhibition across a number of solid and hematologic cancers.
Cell line, Treatment, Time
View SamplesBackground: Systemic inflammation is a whole body reaction that can have an infection-positive (i.e. sepsis) or infection-negative origin. It is important to distinguish between septic and non-septic presentations early and reliably, because this has significant therapeutic implications for critically ill patients. We hypothesized that a molecular classifier based on a small number of RNAs expressed in peripheral blood could be discovered that would: 1) determine which patients with systemic inflammation had sepsis; 2) be robust across independent patient cohorts; 3) be insensitive to disease severity; and 4) provide diagnostic utility. The overall goal of this study was to identify and validate such a molecular classifier. Methods and Findings: We conducted an observational, non-interventional study of adult patients recruited from tertiary intensive care units (ICU). Biomarker discovery was conducted with an Australian cohort (n = 105) consisting of sepsis patients and post -surgical patients with infection-negative systemic inflammation. Using this cohort, a four-gene classifier consisting of a combination of CEACAM4, LAMP1, PLA2G7 and PLAC8 RNA biomarkers was identified. This classifier, designated SeptiCyte Lab, was externally validated using RT-qPCR and receiver operating characteristic (ROC) curve analysis in five cohorts (n = 345) from the Netherlands. Cohort 1 (n=59) consisted of unambiguous septic cases and infection-negative systemic inflammation controls; SeptiCyte Lab gave an area under curve (AUC) of 0.96 (95% CI: 0.91-1.00). ROC analysis of a more heterogeneous group of patients (Cohorts 2-5; 249 patients after excluding 37 patients with infection likelihood possible) gave an AUC of 0.89 (95% CI: 0.85-0.93). Disease severity, as measured by Sequential Organ Failure Assessment (SOFA) score or the Acute Physiology and Chronic Health Evaluation (APACHE) IV score, was not a significant confounding variable. The diagnostic utility o f SeptiCyte Lab was evaluated by comparison to various clinical and laboratory parameters that would be available to a clinician within 24 hours of ICU admission. SeptiCyte Lab was significantly better at differentiating sepsis from infection-negative systemic inflammation than all tested parameters, both singly and in various logistic combinations. SeptiCyte Lab more than halved the diagnostic error rate compared to PCT in all tested cohorts or cohort combinations. Conclusions: SeptiCyte Lab is a rapid molecular assay that may be clinically useful in the management of ICU patients with systemic inflammation.
A Molecular Host Response Assay to Discriminate Between Sepsis and Infection-Negative Systemic Inflammation in Critically Ill Patients: Discovery and Validation in Independent Cohorts.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in DLBCL cell lines as a result of treatment with GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View SamplesWe studied transcriptional changes by Affymetrix human microarrays in 2 DLBCL cell lines as a result of shRNA mediated knockdown of EZH2.
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations.
Specimen part, Cell line, Treatment
View Samples