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Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20553 | GEO | 2010/12/01

SECONDARY ACCESSION(S): PRJNA125195

REPOSITORIES: GEO

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Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array

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.

2010-12-01 | E-GEOD-20553 | biostudies-arrayexpress

Assessing the efficiency and significance of Methylated DNA Immunoprecipitation (MeDIP) assays in using in vitro methylated genomic DNA.

Project description: Not available

| S-EPMC2949662 | biostudies-literature

Clinical and public health research using methylated DNA immunoprecipitation (MeDIP): a comparison of commercially available kits to examine differential DNA methylation across the genome.

Project description: Not available

| S-EPMC3337832 | biostudies-other

Project description:Linkage disequilibrium estimation in Coho salmon

| PRJNA471180 | ENA

Paternally induced transgenerational inheritance of susceptibility to diabetes in mammals (MeDIP-Seq)

Project description:The global prevalence of type 2 diabetes (T2D) is increasing, and it is contributing to the susceptibility to diabetes and its related epidemic in offspring. Although the impacts of paternal T2D on metabolism of offspring have been well established, the exact molecular and mechanistic basis that mediates these impacts remains largely unclear. Here we show that paternal T2D increases the susceptibility to diabetes in offspring through the gametic epigenetic alterations. Paternal T2D led to glucose intolerance and insulin resistance in offspring. Relative to controls, offspring of T2D fathers exhibited altered gene expression patterns in the pancreatic islets, with downregulation of several genes involved in glucose metabolism and insulin signaling pathway. Epigenomic profiling of offspring pancreatic islets revealed numerous changes in cytosine methylation depending on paternal T2D, including reproducible changes in methylation over several insulin signaling genes. Paternal T2D altered overall methylome patterns in sperm, with a large portion of differentially methylated genes overlapped with that of pancreatic islets in offspring. Our study revealed, for the first time, that T2D can be inherited transgenerationally through the mammalian germline by an epigenetic manner. Examination of the effect of paternal T2D on the DNA methylation in the pancreatic islets of offspring and in the sperm of father.

2013-01-02 | E-GEOD-43238 | biostudies-arrayexpress

Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs

Project description:Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced epigenetic DNA methylation changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. We performed MeDIP microarray to examine the changes in DNA promoter methylation during IL13-induced allergic airway inflammation.

2012-04-07 | GSE37079 | GEO

Paternally induced transgenerational inheritance of susceptibility to diabetes in mammals (MeDIP-Seq)

2013-01-02 | GSE43238 | GEO

Mutations and variants of ONECUT1 in diabetes

Project description:Genes involved in distinct diabetes types suggest shared disease mechanisms. We show that rare ONECUT1 coding variants cause monogenic recessive diabetes (neonatal or very early-onset, syndromic) in two unrelated patients, and monogenic dominant diabetes (early adult-onset) in heterozygous relatives of these and 13 additional unrelated cases. Patients heterozygous for rare ONECUT1 coding variants define a subgroup of T2D with early-onset diabetes and other features. In addition, common regulatory ONECUT1 variants are associated with multifactorial T2D. Directed differentiation of human pluripotent stem cells to the pancreatic lineage revealed that loss of ONECUT1 impairs pancreatic progenitor formation and a subsequent endocrine program. We uncovered that ONECUT1 activates the pro-endocrine genes NKX6.1 and NKX2.2 through binding to their cis-regulatory elements. Globally, ONECUT1-directed gene transcription occurs in association with major islet transcription factors, at clusters of pancreas- and endocrine-specific enhancers within open chromatin. ONECUT1 regulates a transcriptional and epigenetic machinery critical for proper endocrine pancreatic development, involved in a spectrum of diabetes, monogenic recessive and dominant, and multifactorial.

2021-11-03 | PXD018887 | Pride

A Bayesian hierarchical model for analyzing methylated RNA immunoprecipitation sequencing data.

Project description: Not available

| S-EPMC8026011 | biostudies-literature

Multiple causal variants underlie genetic associations in humans

Project description:We applied a massively parallel reporter assay (MPRA) in lymphoblastoid cells to functionally evaluate 49,256 allelic pairs, representing 30,893 genetic variants in high, local linkage disequilibrium for 744 independent cis-expression quantitative trait loci (eQTLs) assessed for colocalization across 114 traits.

2021-05-24 | GSE174534 | GEO

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