Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
Project description:We performed ChIP-Seq of H3K27ac in duplicate in both WT and KO mesenchymal stem cells to evaluate global transcriptional changes between the new cells. We identified putative transcription factor binding sites using GEM v1.1 in K27ac data as well as in p MicroRNAs (miRNAs) are small non-coding RNAs that regulates development and disease but induce only moderate repression of directs mRNA targets, suggesting that they coordinate with other modes ofs cellular regulation to effect large changes in gene expression. Ins this work we decouple direct effects of global miRNA loss froms transcriptional changes downstream in a pair of isogenic murines fibroblast cell lines with and without Dicer expression. Wes demonstrate how effects on direct miRNA targets are amplified bys transcription machinery through the construction of a network models that identifies specific transcription factors that cause changes ins mRNA expression upon Dicer loss. Through transcription factors over-expression, we delineate miRNA-mediated transcriptional programss and identify miRNA-mediated coherent and incoherent feed-forwards loops, suggesting a functional role of the interaction between miRNAss and transcription factors. In total, our results indicate thats miRNAs tightly control transcription factors within a denses interconnected network to modulate gene expression. The experiment was designed to mimic the previously captured ChIP-Seq with two replicates in both WT and KO MSCs
Project description:H3K27ac ChIP-seq analysis for WT and Fli-1 KO HSPCs was performed to uncover changes in chromatin H3K27ac modifications following Fli-1 deletion.
Project description:We performed ChIP-seq assay with anti-KAP1 antibodies on Zfp961-GFPflox/flox ESCs.We found KAP1 signal decreased at PBS-Lys sites in Zfp961 KO cells compared to WT, suggesting Zfp961 recruiting KAP1 to ERV-K regions. We performed H3K27ac ChIP on Zfp961 WT or KO mESCs. We found that H3k27ac modification at PBS-Lys sites was elevated upon Zfp961 deletion, indicating Zfp961 serving as a repressive transcription factor.
