Insulin degrading enzyme (IDE) is a major enzyme responsible for insulin degradation in the liver. The modulation of insulin degrading enzyme activity is hypothesized to be a link between T2DM and liver cancer. Results provide insight into role of IDE in proliferation and other cell functions.
Modulation of insulin degrading enzyme activity and liver cell proliferation.
Cell line
View SamplesEffect of sulforaphane (SF) on human colon caco-2 cells after 24h treatment
Transcriptome analysis of human colon Caco-2 cells exposed to sulforaphane.
Specimen part, Disease, Disease stage, Cell line, Compound
View SamplesObesity is characterised by increased adipocyte size and number. Analysis of altered gene expression gives better understading about the mechanisms involved/alterted in the development of obesity in this new obese rat model.
No associated publication
Specimen part
View SamplesObesity is risk factor for development of fatty liver. Analysis of altered gene expression gives better understading about the mechanisms involved/alterted in the development of obesity-induced fattyliver in this new obese rat model.
No associated publication
Specimen part
View SamplesTo evaluate the potential protective effects of APS on intestinal health and its mechanism of action, we performed an RNA sequencing (RNA-seq) study in LPS-stimulated porcine intestinal epithelial cells (IPEC-J2) in vitro
No associated publication
Sex, Specimen part, Cell line
View SamplesSubcutaneous adipose tissue and longissimus dorsi muacle were isolated from Large White pig at 3 days of age, and subcutaneous and intramuscular stromal vascular (SV) cells were obtained as the procedure modified from previous reports. Six Solexa sequencing samples were collected during subcutaneous and intramuscular SV cells adipogenic differentiation at day 0, 2, 4.
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Age, Specimen part
View SamplesBackground and aims: Despite proven clinical efficacy of vedolizumab (VDZ) for inducing and maintaining remission in patients with Crohn's disease (CD) and ulcerative colitis (UC), subgroups of patients have no therapeutic benefit from anti-a4ß7 integrin therapy with VDZ. Within this study, we aimed to identify genetic, cellular and immunological mechanisms that define response and failure to VDZ treatment.Methods: Intestinal RNA Sequencing was performed in UC and CD patients before and at week 14 of VDZ therapy. a4ß7 expression on peripheral and mucosal immune cells was assessed by flow cytometry and immunohistochemistry. Cellular modes of VDZ mediated action were analysed ex vivo and in VDZ treated IBD patients.Results: Transcriptome analysis showed an impairment of signaling cascades associated with adhesion, diapedesis and migration of granulocytes and agranulocytes upon VDZ therapy. In non-remitters to VDZ therapy, a tissue destructive and leucocyte mediated inflammatory activity with activation of TNF dependent pathways was present, all of which were inhibited in remitters to VDZ. Clinical remission was associated with a significant reduction of a4ß7 expression on Th2 and Th17 polarized mucosal CD4+ T cells at week 14 of VDZ therapy and with significantly higher numbers of a4ß7 expressing mucosal cells prior to the initiation of VDZ therapy compared to non-remitters.Conclusions: Intestinal a4ß7 expression prior to VDZ therapy might represent a biomarker that predicts therapeutic response to subsequent VDZ treatment. Due to high activation of TNF signaling in VDZ non-remitters, anti-TNF treatment might represent a promising therapeutic strategy in VDZ refractory patients.
No associated publication
Sex, Specimen part, Disease, Treatment, Subject
View SamplesOur aim was to identify genes that were differentially expressed in microglia stimulated with Lipopolysaccharide, Luteolin, or both.
Luteolin triggers global changes in the microglial transcriptome leading to a unique anti-inflammatory and neuroprotective phenotype.
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View SamplesPU.1 is a key transcription factor for macrophage differentiation. Novel PU.1 target genes were identified by mRNA profiling of PU.1-deficient progenitor cells (PUER) before and after PU.1 activation. We used two different types of Affymetrix DNA-microarrays (430 2.0 arrays and ST 1.0 exon arrays) to characterize the global PU.1-regulated transcriptional program underlying the early processes of macrophage differentiation.
Transcriptomic profiling identifies a PU.1 regulatory network in macrophages.
No sample metadata fields
View SamplesTo define the genes and pathways which are influenced by Foxp1 in the striatum at embryonic stage (E)18.5 we performed a microarray expression study comparing gene expression in striatal tissue from WT and Nestin-Cre (Foxp1-/-) animals.
No associated publication
Specimen part
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