Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We found that ING1b and GADD45a physically and functionally interact in the epigenetic regulation of specific target genes. In order to study this interaction further, we analysed the transcriptional changes in MEF cells from single and double Ing1/Gadd45 knockout mice via microarray profiling. Mouse embryonic fibroblasts (MEF cells) were isolated from embryonic day E15.5 male embryos, either wild-type (WT) or knockout for Ing1 (Ing1-/-), Gadd45a (Gadd45a-/-) or Ing1/Gadd45a (double knockout, DKO), and cultured for 3 passages. Samples were then collected in duplicates per MEF line for expression array profiling.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is required to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the impact of ING1-GADD45a on gene expression, we compared the expression profile of wildtype mouse embryonic fibroblasts (MEFs) with Ing1- and Gadd45a- single- or double-knockout (DKO) MEFs.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is required to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the impact of ING1-GADD45a on MEF-to-adipocyte differentiation, we compared the gene expression profile of wildtype mouse embryonic fibroblasts (MEFs) with Ing1- and Gadd45a- single- or double-knockout (DKO) MEFs at day 6 of adipogenic differentiation via RNA-sequencing.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the physiological impact of ING1-GADD45a on DNA methylation in base-resolution genome-wide, we compared the methylation levels of wildtype mouse embryonic fibroblasts (MEFs) with Ing1/Gadd45a double-knockout MEFs via whole genome bisulfite sequencing.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We found that ING1b and GADD45a physically and functionally interact in the epigenetic regulation of specific target genes. In order to study this interaction further, we analysed the transcriptional changes in MEF cells from single and double Ing1/Gadd45 knockout mice via microarray profiling.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. Hence, GADD45a and ING1 play a crucial role in epigenetic gene regulation. In order to study the physiological role of ING1-GADD45a on gene expression regulation, we compared the expression profiles of white adipose tissue (WAT) from wildtype, Ing1-/-, Gadd45-/- and double-knockout (DKO) mice.
Project description:ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the physical interaction of distant GADD45a and ING1 bound regions, we performed multiplexed NG Capture-C chromatin conformation capture assay in wildtype and knockout mouse embryonic fibroblasts.
Project description:GADD45a is a nuclear protein involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that GADD45a physically and functionally interacts with TET1 to mediate active DNA demethylation and is recruited by ING1 to its target sites. In this study, we identified GADD45a bound genomic loci in mouse embryonic fibroblasts (MEFs) via ChIP-Sequencing.
