Microarrays were used to analyze the gene expression in endoscopic-derived intestinal mucosal biopsies from patients with inflammatory bowel diseas (IBD) and controls
Genetic and Transcriptomic Bases of Intestinal Epithelial Barrier Dysfunction in Inflammatory Bowel Disease.
Specimen part, Disease
View SamplesPrdm12, a novel key regulator of the Nerve Growth Factor-TrkA signaling pathway, is required for nociceptive sensory neuron development Overall design: RNA-seq analysis in triplcate of the transcriptome of thoracic dorsal root ganglia with associated spinal cord of E11.5 Prdm12 KO and WT embryos.
Prdm12 Directs Nociceptive Sensory Neuron Development by Regulating the Expression of the NGF Receptor TrkA.
Specimen part, Cell line, Subject
View SamplesMicroarrays were used to investigate the the effect of vedolizumab (VDZ) therapy on colonic mucosal gene expression in UC patients and compared the changes to those observed with infliximab (IFX) therapy.
Effect of vedolizumab (anti-α4β7-integrin) therapy on histological healing and mucosal gene expression in patients with UC.
Specimen part
View SamplesWe used microarrays to identify mucosal gene signatures predictive of response to infliximab (IFX) in patients with inflammatory bowel disease (IBD) and to gain more insight into the pathogenesis of IBD.
Mucosal gene expression of antimicrobial peptides in inflammatory bowel disease before and after first infliximab treatment.
Specimen part, Disease
View SamplesIncreased levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) have been detected in fibrotic strictures in Crohns disease. In a murine model of chronic inflammation, fibrosis was associated with an increase in TIMP-1 and inhibition of matrix metalloproteinase (MMP)-mediated degradation. We investigated the effect of TIMP-1 deficiency on the colonic gene expression in acute and chronic murine models of colitis, using whole genome gene expression arrays.
Genetic Deletion of Tissue Inhibitor of Metalloproteinase-1/TIMP-1 Alters Inflammation and Attenuates Fibrosis in Dextran Sodium Sulphate-induced Murine Models of Colitis.
No sample metadata fields
View SamplesFibroblasts from PRDM12 patients and unaffected wildtype relatives were cultured until near confluency. The transcriptional profile of those cells was determined by mRNA sequencing and uncovered differential expression in several known pain and neurodevelopmental genes. Overall design: Transcriptome comparison of human PRDM12 mutant and wildtype fibroblasts
The evolutionarily conserved transcription factor PRDM12 controls sensory neuron development and pain perception.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrated miRNA and mRNA expression profiling in inflamed colon of patients with ulcerative colitis.
Specimen part, Disease
View SamplesThe lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease.
Unique gene expression and MR T2 relaxometry patterns define chronic murine dextran sodium sulphate colitis as a model for connective tissue changes in human Crohn's disease.
Sex, Age, Specimen part
View SamplesIn this study, we investigated if miRNA expression in UC mucosa is altered and correlated our findings with mucosal mRNA expression. Integration of mRNA and miRNA expression profiling may allow the identification of functional links between dysregulated miRNAs and their predicted target mRNA.
Integrated miRNA and mRNA expression profiling in inflamed colon of patients with ulcerative colitis.
Specimen part, Disease
View SamplesDNA methylation is a dynamic epigenetic modification that plays a key role in various cellular processes. Proteins that bind to DNA depending on its methylation status are thought to play an important role in DNA methylation-mediated gene expression. Using a variety of genomics and proteomics approaches, we identified ZBTB2 as a novel reader of unmethylated DNA. ZBTB2, which forms a complex with ZBTB25 and ZNF639, preferentially binds at CpG island promoters in mouse embryonic stem cells, from where it regulates genes that are involved in the exit from pluripotency. Binding of ZBTB2 to target genes is mostly associated with gene activation. Furthermore, ZBTB2 is intricately interwoven with DNA methylation, as we found not only that its binding to DNA is methylation-sensitive, but also that ZBTB2 regulates the turnover of methylated DNA. Summarising, we propose that ZBTB2 is a DNA methylation-sensitive transcription factor that is involved in cellular differentiation. Overall design: RNA-seq samples of wildtype ESCs and Zbtb2 KO ESCs
ZBTB2 reads unmethylated CpG island promoters and regulates embryonic stem cell differentiation.
Specimen part, Subject
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