Project description:In this study, we demonstrated dysregulation of DNA transcription in H3K4me3 histone in circulating neutrophils of HIV-infected subjects. Chromatin immunoprecipitation sequencing (ChIPseq) H3K4me3 histone analysis revealed that the most spectacular abnormalities were observed in the exons, introns and promoter-TSS regions. Bioinformatic analysis of Gene Ontology, including biological processes, molecular function and cellular components, demonstrated that the main changes were related to the genes responsible for cell activation, cytokine production, adhesive molecule expression, histone remodeling via upregulation of methyltransferase process and downregulation of NF-kB transcription factor in canonical pathways. Abnormalities within H3K4me3 implicated LPS-mediated NF-kB canonical activation pathway that was a result of low amounts of kB DNA sites within histone H3K4me3, low NF-kB (p65 RelA) and TLR4 mRNA expression as well as reduced free NF-kB (p65 RelA) accumulation in the nucleus. ‘Panoramic view of the landscape gene’ within histone H3K4me3 led us postulate that impairment within the canonical NF-kB cell activation pathway may be the primary phenomenon responsible for neutrophil dysfunction observed in HIV-infected individuals
Project description:This dataset has been generated to identify promoter regions in the chicken genome to distinguish active and inactive genes. We focussed our analyses on actively transcribed tRNA and mRNAs genes. Chicken liver was cross-linked to capture histone-DNA interactions. Sequencing libraries were prepared from H3K4me3-precipitated DNA and input control.
Project description:To determine the positions of promoters and enhancers in developing Xenopus laevis epithelial progenitors, we performed ChIPseq on the histone modifications H3K4me3 and H3K27ac. We also performed ChIPseq on the transcription factors foxj1 (in the presence or absence of rfx2), myb (in the presence or absence of multicilin), and rad21. Some embryos were harvested as wild-types; in other experiments, we injected embryos with mRNAs encoding FLAG-foxj1 (with and without rfx2 morpholino) or GFP-myb (with and without an inducible form of multicilin (mcidas-HGR)). We then isolated epithelial progenitors surgically and, when injected with multicilin, induced at mid-stage 11. We then harvested chromatin at 9 hours after induction (roughly stage 18) and performed ChIPseq using antibodies against endogenous targets (H3K4me3, H3K27ac, rad21) or protein tags (FLAG, GFP). We then sequenced these libraries, aligned the reads to the X. laevis genome (version 9.1) with bwa mem and called peaks with HOMER, using input as background.
Project description:To determine the positions of promoters and enhancers in developing Xenopus laevis epithelial progenitors, we performed ChIPseq on the histone modifications H3K4me3 and H3K27ac. We also performed ChIPseq on the transcription factors foxj1 (in the presence or absence of rfx2), myb (in the presence or absence of multicilin), and rad21.
Project description:ChIPseq data for human glioblastoma patients, EGAS00001003953. Mix of input, H3K27ac, H3K27me1, H3K27me3, H3K36me3, H3K4me1, H3K4me3, H3K9me3 and BRD, 20 human samples, 2 cell lines (LN229, ZH487).
