Project description:We measured the methylation levels of gene promoters of cerebral cortex of mice. We used MeDIP-array, immunoprecipitating genomic DNA with an antibody against methylated DNA and measuring methylation levels using custom arrays. The input DNA was used as control.
Project description:Custom array designed to tile Linkage Disequilibrium Blocks of T2D GWAS SNPs, monogenic candidates for T2D and Obesity, and all plausible imprinted loci from human and mouse data. Case Control comparison of MeDIP for Type 2 Diabetes. MeDIP versus Input fraction.
Project description:Epigenetics was reported to mediate the effects of environmental risk factors on disease pathogenesis. To unleash the role of DNA methylation modification in the pathological process of cardiovascular diseases in diabetes, we screened differentially methylated genes by methylated DNA immunoprecipitation chip (MeDIP-chip) among the enrolled participants.
Project description:CpG methylation analysis of MeDIP DNA using Agilent Human DNA methylation Microarray slides (G4495A, AMADID 023795) Using methylated DNA immunoprecipitation microarray (MeDIP-chip) and Agilent Human DNA methylation Microarray slides (G4495A, AMADID 023795) we report genomic methylation signatures of tissues resected from Mesial temporal epilepsy (MTLE) and Focal cortical dysplasia (FCD) type II patients undergoing surgery. Control samples were obtained from the non-epileptic post mortem cases without any brain pathology
Project description:Genomic imprinting describes the expression of a subset of mammalian genes from one parental chromosome. The parent-of-origin specific expression of imprinted genes relies on DNA methylation of CpG-dinucleotides at differentially methylated regions (DMRs) during gametogenesis. We identified the paternally methylated DMRs at mouse chromosome 1 near the imprinted Zdbf2 gene using a methylated-DNA immunoprecipitation-on-chip (meDIP-on-chip) method applied to DNA from parthenogenetic (PG)- and androgenetic (AG)-derived cells and sperm. To identify novel DMRs, genome-wide methylation analysis of three samples were performed using MeDIP and whole genome tiling array.
Project description:Genomic imprinting describes the expression of a subset of mammalian genes from one parental chromosome. The parent-of-origin specific expression of imprinted genes relies on DNA methylation of CpG-dinucleotides at differentially methylated regions (DMRs) during gametogenesis. We identified the paternally methylated DMR at human chromosome 2 near the imprinted ZDBF2 gene using a methylated-DNA immunoprecipitation-on-chip (meDIP-on-chip) method applied to DNA from sperm. To analyze whether or not the GPR1-ZDBF2 DMR is conserved in human genome, methylation analysis of human sperm sample was performed using MeDIP and genome tiling array.
Project description:We measured the methylation levels of gene promoters of cerebral cortex of mice. We used MeDIP-array, immunoprecipitating genomic DNA with an antibody against methylated DNA and measuring methylation levels using custom arrays. The input DNA was used as control. triplicates of frontal cortex DNA pools of 3 mice
Project description:We analyzed the cell free DNA methylomes using 14 plasma samples from patients with mCRPC in the Barrier cohort. Methylation was profiled using the methylated DNA immunoprecipitation coupled to next generation sequencing (MeDIP) technology.
Project description:The actions of environmental toxicants and relevant mixtures in promoting the epigenetic transgenerational inheritance of ovarian disease was investigated with the use of a fungicide, a pesticide mixture, a plastic mixture, dioxin and a hydrocarbon mixture. After transient exposure of an F0 gestating female rat during embryonic gonadal sex determination, the F1 and F3 generation progeny adult onset ovarian disease was assessed. Transgenerational disease phenotypes observed included an increase in cysts resembling human polycystic ovarian disease (PCO) and a decrease in the ovarian primordial follicle pool size resembling primary ovarian insufficiency (POI). The F3 generation granulosa cells were isolated and found to have a transgenerational effect on the transcriptome and epigenome (differential DNA methylation). Epigenetic biomarkers for environmental exposure and associated gene networks were identified. Epigenetic transgenerational inheritance of ovarian disease states was induced by all the different classes of environmental compounds, suggesting a role of environmental epigenetics in ovarian disease etiology. Granulosa cells from large antral follicles were collected and evaluated from F3 generation rats that were ancestrally exposed to one of the five different treatments: Vinclozolin, Pesticide (includes permethrin and DEET), Plastics (includes BPA, DBP and DEHP), Low-dose Plastics (50% of Plastics dose), Dioxin, Hydrocarbon (Jet fuel JP8), or DMSO vehicle as Control. Vinclozolin lineage alterations in differentially DNA methylated regions (DMR) in the granulosa cells was investigated by using a methylated DNA immunoprecipitation (MeDIP) procedure followed by comparative hybridization on a genome wide promoter tiling array (Chip), termed an MeDIP-Chip assay. The DNA fractions from four animals of the same treatment group were pooled to create three different pooled DNA samples from each of the two treatment groups (experimental vs. control). These DNA samples were then used for methylated DNA immunoprecipitation (MeDIP) using Nimblegen microarrays. Each MeDIP sample was then used to preform three different comparative (amplified MeDIP vs. amplified MeDIP) hybridization experiments (3 sub-arrays), each encompassing DNA samples from 24 animls (3 treatment and 3 control groups).