2a55ff79-e333-4e5c-b9cb-854fbf65deb3 - samples
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ABSTRACT:
PROVIDER: EGAD00001005205 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:14 ChIP-Seq datasets of H3K27ac in human pancreatic islets from 14 donors, where islets were treated in high (11mM) glucose conditions. Samples IDs HI-129, HI-130, HI-131, HI-132, HI-135, HI-137 and HI-152 were also cultured in low glucose conditions.
| EGAD00001005204 | EGA
Project description:7 RNA-Seq datasets in human pancreatic islets from 7 donors, where islets were treated in high (11mM) glucose conditions
| EGAD00001005207 | EGA
Project description:7 RNA-Seq datasets in human pancreatic islets from 7 donors, where islets were using low (4mM) glucose conditions.
| EGAD00001005208 | EGA
Project description:3 ChIP-Seq datasets of Cohesin in human pancreatic islets from 3 donors
| EGAD00001005203 | EGA
Project description:6 ChIP-Seq datasets of Mediator in human pancreatic islets from 6 donors
| EGAD00001005202 | EGA
Project description:<p>In this study we profile the epigenomic enhancer landscapes of CLL B cells (CD19+/CD5+) harvested from peripheral blood of patients from our Center. Included are results of ChIPseq profiling using chromatin immunoprecipitation of the enhancer histone mark H3K27ac (acetylated lysine 27 on histone H3), and open chromatin profiles using ATAC-seq (assay for transposase accessible chromatin). These profiles are used to define the global enhancer and super enhancer landscape of CLL B cells, and to derive active transcription factor networks associated with this disease. Also included are H3K27ac ChIP-seq and ATAC-seq datasets for non-CLL B cells obtained from the peripheral blood of normal adult donors.</p>
| phs001704 | dbGaP
Project description:13 ATAC-Seq datasets of human pancreatic islets from 13 donors
| EGAD00001005201 | EGA
Project description:Enhancers are fundamental to gene regulation. Post-translational modifications by the small ubiquitin-like modifiers (SUMO) modify chromatin regulation enzymes, including histone acetylases and deacetylases. However, it remains unclear whether SUMOylation regulates enhancer marks, acetylation at the 27th lysine residue of the histone H3 protein (H3K27Ac). We hypothesize that SUMOylation regulates H3K27Ac. To test this hypothesis, we performed genome-wide ChIP-seq analyses. We discovered that knockdown (KD) of the SUMO activating enzyme catalytic subunit UBA2 reduced H3K27Ac at most enhancers. Bioinformatic analysis revealed that TFAP2C-binding sites are enriched in enhancers whose H3K27Ac was reduced by UBA2 KD. ChIP-seq analysis in combination with molecular biological methods showed that TFAP2C binding to enhancers increased upon UBA2 KD or inhibition of SUMOylation by a small molecule SUMOylation inhibitor. However, this is not due to the SUMOylation of TFAP2C itself. Proteomics analysis of TFAP2C interactome on the chromatin identified histone deacetylation (HDAC) machinery. TFAP2C KD reduced HDAC binding to chromatin and increased H3K27Ac marks at enhancer regions, suggesting that TFAP2C is involved in recruiting HDAC. Taken together, our findings provide important insights into regulation of enhancer marks by SUMOylation.
2024-04-13 | PXD045644 | Pride
Project description:C57BLKS/J mice are susceptible to diabetes, because of islet dysfunction, whereas C57BL6/J mice are not. Differences in gene expression between the two strains may account for this sensitivity. Furthermore these differences may only be evident in the hyperstimulated (diabetic or hyperglycemic) state. To this end profiling islets from these two strains cultured in both low and high glucose may reveal the underlying mechanism. Keywords: Mouse strain comparison under different culture conditions In the study presented here, pancreatic islets from 20 mice grown in low and high glucose conditions were assayed for differences in gene expression. (five C57BLKS/J low glucose, four C57BLKS/J high glucose, six C57BL6/J low glucose, five C57BL6/J high glucose). Technical replicates are achieved by labeling each sample with both Cy3 and Cy5, and combining the values for each hybridization.
2008-12-30 | E-GEOD-11257 | biostudies-arrayexpress
Project description:Objectives: Glycine acts in an autocrine positive feedback loop in human β cells through its ionotropic receptors (GlyRs). In type 2 diabetes (T2D), islet GlyR activity is impaired by unknown mechanisms. We sought to investigate if the GlyR dysfunction in T2D is replicated by hyperglycemia per se, and to further characterize its action in β cells and the islets. Methods: GlyR-mediated currents were measured using whole-cell patch-clamp in human β cells from donors with or without T2D, or after high glucose culture. We also correlated glycine-induced current amplitude with transcript expression levels through patch-seq. The expression of the GlyR α1, α3, and β subunit mRNA splice variants was compared between islets from donors with and without T2D, and after high glucose culture. Insulin secretion from human islets was measured in the presence or absence of the GlyR antagonist strychnine. Results: Gene expression of GlyRs was decreased in islets from T2D donors along with smaller GlyR-mediated currents in the β cells. Glycine-induced currents are also reduced in islets from donors without diabetes after 48 hours of culture in high glucose, along with reducedα1 subunit expression and increased α3 subunit expression. Glycine-evoked currents are highly heterogeneous between different β cells within and between donors; inversely correlated with donor HbA1c; and significantly correlated to the expression of 99 different transcripts. Finally, glucose-stimulated insulin secretion is decreased in the presence of strychnine.
2024-12-02 | GSE280267 | GEO