We defined the C/EBPa signature characterized by a set of genes which are upregulated upon C/EBPa activation. In order to identify the C/EBPa signature, we performed microarray gene expression analysis of K562 cells stably expressing p42-C/EBPa-ER after activating the C/EBPa construct to translocate to the nucleus for 6 hours with beta-estradiol.
The gene signature in CCAAT-enhancer-binding protein α dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors.
Cell line, Treatment
View SamplesTranscriptome levels of matched patient-derived xenograft (PDX) in vitro-in vivo models. Overall design: Comparison of gene expression levels between matched patient-derived xenograft in vitro-in vivo models.
Generation of matched patient-derived xenograft in vitro-in vivo models using 3D macroporous hydrogels for the study of liver cancer.
Specimen part, Disease, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
LPS independent activation of the pro-inflammatory receptor Trem1 by C/EBPε in granulocytes.
Specimen part
View SamplesTo identify target genes of C/EBPepsilon in differentiated granulocytes, total RNA were purified from sorted Gr-1intermediate/Mac-1+ and Gr-1hi/Mac-1+ cells of C/EBPepsilon knock out and C57BL/6 wild type mice using RNeasy Mini Kit (Qiagen). The differences of their expression pattern were compared with Illumina Mouse WG-6v2 Expression Chip platform. Raw Illumina BeadArray data in IDAT format were preprocessed using the open-source Bioconductor package illuminaio with the Illumina array design formation BGX file downloaded from NCBI, GEO accession: GPL6887. Following the preprocessing, the expression data were normalized by applying control background correction, log transformation and inter-quantile normalization using the neqc function from the limma bioconductor package. This allowed us to compare the transcriptomic consequences of C/EBPepsilon in two independent populations.
LPS independent activation of the pro-inflammatory receptor Trem1 by C/EBPε in granulocytes.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line, Treatment
View SamplesWe used the microarray analysis to detail the gene expression profile from the leukemic cell line HL-60
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line
View SamplesIdentification of the all RNA species associated with DNMT1. Using a comparative genome-scale approach we identified and correlated the RNA species physically associated with DNMT1 and proximal to the annotated genes to the methylation status of the corresponding loci and expression levels of the respective genes. This comparative approach delineated the first -DNMT1 centered- 'epitranscriptome' map, a comprehensive map cross-referencing DNMT1-interacting transcripts to (i) DNA methylation and (ii) gene expression profile. Overall design: Relationship between DNMT1-RNA interactions, DNA methylation and gene expression
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line, Subject
View SamplesComplement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection.
C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.
Specimen part, Treatment
View SamplesUsing the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice autoimmune indications. However, our current knowledge of the role of BTK in immune competence has been gathered in the context of genetic inactivation of btk in both mice and man. Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice. We implicate BTK in tonic BCR signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity, and find that B1 cells survive and function independently of BTK. While BTK inhibition does not impact humoral memory survival, antigen-driven clonal expansion of memory B cells and antibody secreting cell generation are inhibited. These data define the role of BTK in the mature immune system and mechanistically predict the clinical phenotype of BTK inhibition.
Modeling the clinical phenotype of BTK inhibition in the mature murine immune system.
Specimen part
View SamplesIdentification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro.
Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression.
Specimen part
View Samples