Project description:In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a mouse insulinoma cell line and measured the regulated expressed genes by RNA-seq. We have shown that Zac1 regulates many genes belonging to the Imprinted Gene Network, including genes coding for the extra-cellular matrix.
Project description:In order to determine the targets of the imprinted transcription factor Zac1, we compared wild type and Zac1-mutant MEFs and measured the differentially expressed genes by RNA-seq. Genes deregulated in the absence of Zac1 include genes belonging to the Imprinted Gene Network and genes coding for the extra-cellular matrix.
Project description:In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a neuroblastoma cell line and measured both the regulated expressed genes by Differential Gene Expressed analysis and Zac1 binding sites throughout the mouse genome by ChIP-seq. We have shown that Zac1 regulates and binds closed to many genes belonging to the Imprinted Gene Network.
Project description:In order to determine the imprinted transcription factor Zac1 targets, we overexpressed Zac1 in a neuroblastoma cell line and measured both the regulated expressed genes by Differential Gene Expressed analysis and Zac1 binding sites throughout the mouse genome by ChIP-seq. We have shown that Zac1 regulates and binds closed to many genes belonging to the Imprinted Gene Network.
Project description:Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes.
Project description:A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation
Project description:Genome-wide characterization of Zac1 target genes reveals its role as a broad regulator of the imprinted gene network including extracellular matrix genes
Project description:The aim of the study was to investigate whether the trefoil peptide genes, in concerted action with a miRNA regulatory network, were contributing to nutritional maintrenance. Using a Tff3 knock-out mouse model, 21 specific miRNAs were noted to be significantly deregulated when compared to the wild type strain.
