Project description:In this study, we aimed at determining RNA interactors of L1TD1 RNPs. To achieve this, DNMT1 KO and DNMT1 L1TD1 DKO HAP1 cells were generated by Crispr/Cas9 gene editing tool and L1TD1 RIP was performed by using these cell lines. Our study reveals a comprehensive analysis of differentially enriched transcripts in L1TD1 containing RNPs.
Project description:In this study, we aimed at analyzing gene expression profile of DNMT1 KO and DNMT1 L1TD1 DKO HAP1 cells using high throughput sequencing. Our study reveals a comprehensive analysis of differentially expressed transcripts in the absence of L1D1.
2025-01-01 | GSE254460 | GEO
Project description:Gene expression profile of DNMT1 KO and DNMT1 L1TD1 DKO HAP1 cell lines
Project description:The objectives of this study are to understand the regulatory roles of MAZ in biological processes using the NGS-deriveed ChIP-seq, DNA-MEDIP-seq and RNA-seq data in HAP1 control cells and MAZ knockout cells. Our comparative analysis of these data generated from the HAP1 control and MAZ KO cells shows that MAZ is required for recruiting STAT1 to its target sites by reshaping epigenetic landscape in the human genome, thereby mediating antiviral response cells. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for STAT1 and H3K4me3, H3K27Ac in HAP1 cells.
Project description:We performed a genome-scale screen for suppressors of interferon stimulated gene (ISG) expression in human haploid cells (HAP1). Ubiquitin specific peptidase 14 (USP14) was a significant hit. In order to validate USP14 as a regulator of ISG expression, we created knockouts of USP14 in HAP1 cells using CRISPR-Cas9 and performed RNA-seq on coding RNA from USP14 KO and WT cells. This data was used to determine if ISGs were upregulated in USP14 KO HAP1 cells.
Project description:We performed a genome-scale screen for suppressors of interferon stimulated gene (ISG) expression in human haploid cells (HAP1). DEAD-box helicase 6 (DDX6) was a significant hit. In order to validate DDX6 as a regulator of ISG expression, we created knockouts of DDX6 in HAP1 cells using CRISPR-Cas9 and performed RNA-seq on coding RNA from DDX6 KO and WT cells. This data was used to determine if ISGs were upregulated in DDX6 KO HAP1 cells.
Project description:The objectives of this study are to understand the regulatory roles of MAZ in biological processes using the NGS-deriveed ChIP-seq, DNA-MEDIP-seq and RNA-seq data in HAP1 control cells and MAZ knockout cells. Our comparative analysis of these data generated from the HAP1 control and MAZ KO cells shows that MAZ is required for recruiting STAT1 to its target sites by reshaping epigenetic landscape in the human genome, thereby mediating antiviral response cells. MEDIP-seq was performed using the MagMeDIP-seq Package from Diagenode in HAP1 control and HAP1 MAZ knockout cells following manufacturer's instructions.
Project description:This data includes regulatory factor profiling using DNase and ChIP-seq and methylation profiling using bisulfite-seq. We investigated CTCF occupancy in the context of reduced methylation by performing genome-wide profiling with chromatin immunoprecipitation (ChIP-seq) in HCT116 cells and DNMT1 and DNMT3B double knockout (DKO) HCT116 cells. We also profiled HCT116 and DKO using DNaseI-seq and ChIP-seq for trimethylation of histone 3 lysine 4 (H3K4me3) and acetylation of histone 3 lysine 27 (H3K27ac), Finally, we performed ChIP-seq on 3 replicates of mock-treated and 2 replicates of 5-aza-CdR-treated K562 cells.
