Project description:We benchmark Illumina’s HiseqX10 instrument against Beijing Genomics Institute’s (BGI) DNBSEQ-G400 platform, a considerably cheaper sequencing alternative. For comparisons, the same bulk ATAC-seq libraries generated from pluripotent stem cells (PSCs) and fibroblasts were sequenced on both platforms. Both instruments generate sequencing reads with comparable mapping rates and genomic context. However DNBSEQ-G400 data contained a significantly higher number of small, sub-nucleosomal reads (>30% increase) and a reduced number of bi-nucleosomal reads (>75% decrease), which resulted in narrower peak-bases and improved peak calling, enabling the identification of 4% more differentially accessible regions between PSCs and fibroblasts. Ability to identify master TFs that underpin the PSC state relative to fibroblasts, including aggregate and de novo foot-printing capacity, were highly similar between data generated on both platforms.
Project description:We benchmark Illumina’s HiseqX10 instrument against Beijing Genomics Institute’s (BGI) DNBSEQ-G400 platform, a considerably cheaper sequencing alternative. For comparisons, the same bulk ATAC-seq libraries generated from pluripotent stem cells (PSCs) and fibroblasts were sequenced on both platforms. Both instruments generate sequencing reads with comparable mapping rates and genomic context. However DNBSEQ-G400 data contained a significantly higher number of small, sub-nucleosomal reads (>30% increase) and a reduced number of bi-nucleosomal reads (>75% decrease), which resulted in narrower peak-bases and improved peak calling, enabling the identification of 4% more differentially accessible regions between PSCs and fibroblasts. Ability to identify master TFs that underpin the PSC state relative to fibroblasts, including aggregate and de novo foot-printing capacity, were highly similar between data generated on both platforms.
Project description:This study presents RNA-sequencing data from Human Primary Dermal Fibroblast, Neonatal (HDFn) cells treated with four phosphodiesterase (PDE) inhibitors—roflumilast, rolipram, cilostazol, and milrinone—across a 2-fold serial dilution range spanning from 7.8 nM to 8,000 nM. The dataset includes biological replicates for each treatment condition and dose. Total RNA was extracted and sequenced on the DNBSEQ-G400 platform. The processed data includes gene-level read counts and differential gene expression results. This dataset enables dose-dependent transcriptional profiling of PDE inhibitors, providing a resource for drug response and perturbation signature analysis.
Project description:This study investigates transcriptomic alterations associated with pancreatic ductal adenocarcinoma (PDAC) progression in genetically engineered mouse models. Total RNA was extracted from two types of samples: (1) pancreatic cancer cells isolated from KPC and KPNiC tumors, and (2) whole pancreatic tissue lysates from WT, NiC, KC, and KNiC mice. RNA-seq libraries were polyA-selected and strand-specific, sequenced on the DNBSEQ-G400 platform (BGI Genomics). Bioinformatic analyses included read alignment (HISAT2), quantification (RSEM), differential gene expression (DESeq2), and gene set enrichment analysis (GSEA). This dataset provides insights into the impact of NIK deletion on pancreatic tumor biology.
Project description:Purpose: DCIR is an inhibitory type of C-type lectin receptor that regulates DC functions. This study aimed to find the genes that could be regulated through DCIR. Method: Splenic DCs from WT and Dcir-/- mice were colutured with T cells that express specific TCR for MOG35-55 for 3 days in the presence of MOG peptide. CD11c+ cells were collected by an auto MACS. RNA profiles were generated by deep sequencing, in triplicate, using DNBSEQ-G400. Results: We detected xxx gense that were higher expression in Dcir-/- DCs, compared with WT DCs, with a fold change ≥1.5 and p value <0.05. Conclusion: Our data showed that Dcir deficiency in DCs changed the gene expression pattern, compared to WT DCs, in the coculture system of T cells. DCIR regulates the expression of DC genes that are associated with the functions of DCs.
