Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10276357.fastq.gz | Fastqsanger.gz | |||
| SRR10276358.fastq.gz | Fastqsanger.gz | |||
| SRR10276359.fastq.gz | Fastqsanger.gz | |||
| SRR10276360.fastq.gz | Fastqsanger.gz | |||
| SRR10276361.fastq.gz | Fastqsanger.gz |
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Project description:Founder mice islet RNA profiling
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Project description:To get a more complete picture of the transcriptional changes associated with Pdx1 loss in ?-cells, we conducted an mRNA microarray comparing normal islet ?-cells and a-cells to the reprogrammed cells from PKO mice. Islet beta cells are from mice which has a single copy of Pdx1 flox (Pdx1L/+) allele, but is considered normal based on normal islet morphology, gene profiling, and euglycemic status. We chose to use heterozygous mice as control to avoid the litter effect. Islet alpha cells are from normal mice. To enrich for genes directly affected by Pdx1 loss, we chose the early time-point for analysis of PKO mice (5d after TAM administration). Control mRNA profiling was performed on FACS sorted islet YFP+ ?-cells and a-cells obtained from 2 month-old glucagon-Cre; RosaYFP and RIP-CreER; Pdx1fl/+, RosaYFP mice, respectively.
2013-11-19 | E-GEOD-52258 | biostudies-arrayexpress
Project description:ob/ob mice on pancreatic islet
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Project description:We knocked out the critical autophagy enzyme, ATG7, in the β-cells of mice (ATG7Δβ-cell) then monitored blood glucose to assess the phenotype induced by this KO model. We found that all ATG7Δβ-cell mice developed diabetes between 11-15 weeks of age. We isolated islets from ATG7Δβ-cell and littermate control mice several weeks prior to diabetes development (7-10 weeks of age) and performed bulk islet proteomics. The purpose of this experiment was to understand the islet biological process pathways altered by dysfunctional β-cell autophagy in the ATG7Δβ-cell model.
2025-01-22 | PXD060032 | Pride
Project description:To get a more complete picture of the transcriptional changes associated with Pdx1 loss in β-cells, we conducted an mRNA microarray comparing normal islet β-cells and a-cells to the reprogrammed cells from PKO mice. Islet beta cells are from mice which has a single copy of Pdx1 flox (Pdx1L/+) allele, but is considered normal based on normal islet morphology, gene profiling, and euglycemic status. We chose to use heterozygous mice as control to avoid the litter effect. Islet alpha cells are from normal mice.
2013-11-19 | GSE52258 | GEO
Project description:Identifying cis-regulatory elements is important to understand how human pancreatic islets modulate gene expression in physiologic or pathophysiologic (e.g., diabetic) conditions. We conducted genome-wide analysis of DNase I hypersensitive sites, histone H3 lysine methylation marks (K4me1, K4me3, K79me2), and CCCTC factor (CTCF) binding in human islets. This identified ~18,000 putative promoters (several hundred novel and islet-active). Surprisingly, active promoter marks were absent at genes encoding islet-specific hormones, suggesting a distinct regulatory mechanism. Of 34,039 distal (non-promoter) regulatory elements, 47% are islet-unique and 22% are CTCF-bound. These findings present a global snapshot of the human islet epigenome and should provide functional context for non-coding variants emerging from genetic studies of T2D and other pancreatic islet disorders. Three different islet samples were tested for DNase I hypersensitivity by DNase-Seq. Five different primary pancreatic islet samples were evaluated for several chromatin modifications (H3K4me3, H3K4me1, H3K79me2) by ChIP-seq. One islet sample was evaluated for CTCF binding via ChIP-seq, All ChIP-seq samples have both non-specific IP (GFP) and input DNA controls.
2010-11-02 | E-GEOD-23784 | biostudies-arrayexpress
Project description:We performed a global gene expression analysis comparing intragraft tolerant CD8+ T cells from CD3 antibody-treated mice showing permanent islet graft survival to intra-graft effector CD8+ T cells isolated from untreated mice showing acute rejection of islet allografts. The objective was to emphasize the anergic profile of CD8+ T cells residing within the pancreatic islet allograft of mice rendered tolerant following CD3 antibody therapy.
2017-02-10 | GSE68208 | GEO
Project description:Hyperinsulinemia often precedes type 2 diabetes but its role in disease progression is unknown. Palmitoylation, a protein modification implicated in regulated exocytosis, is reversed by acyl-protein thioesterase 1 (APT1). We found altered APT1 biology in pancreatic islets from humans with type 2 diabetes, and APT1 knockdown in nondiabetic human islets caused insulin hypersecretion. Chow fed global and islet specific APT1 knockout mice had enhanced glucose tolerance due to islet autonomous increased glucose-stimulated insulin secretion. APT1 deficiency did not affect islet calcium dynamics but prolonged insulin granule fusion. Using palmitoylation proteomics, we identified Scamp1 as an APT1 substrate that localized to insulin secretory granules. Knockdown of Scamp1 caused insulin hypersecretion. APT1 deficient insulinoma cells subjected to nutrient excess had increased apoptosis, and expression of a mutated Scamp1 incapable of being palmitoylated in APT1 deficient cells rescued insulin hypersecretion and nutrient induced apoptosis. Compared to APT1 sufficient controls, high fat fed islet specific APT1 knockout mice and global APT1 deficient db/db mice showed increased -cell failure. These findings suggest that the depalmitoylation enzyme APT1 is regulated in human islets, and that APT1 deficiency causes insulin hypersecretion leading to -cell failure, modeling the evolution of some forms of human type 2 diabetes.
2023-11-05 | PXD038554 | Pride