Project description:Three independent repeats of ChIP-seq from THP-1 after 24h treatment with 1,25D or EtOH (control), using antibodies against histone markers H3K27ac and H3K4me3
Project description:Three independent repeats of ChIP-seq from THP-1 after 2h and 8h treatment with 1,25D or EtOH (control), using antibody against histone marker H3K4me3.
Project description:Macrophages with innate immune memory are in a modified steady-status with altered responsiveness to stimulation featured by rewired epigenetic program. To better convey the concept of IGF-2-mediated innate immune memory and help understanding the anti-inflammatory responsiveness of macrophages, we analyzed histone modifications (H3K4me1, H3K4me3, and H3K27ac) by whole genome chip-sequencing analysis in control macrophages and IGF-2-preprogrammed macrophages. In the whole genome chip-sequencing analysis, we found that IGF-2 has limited effects on H3K4me1and H3K4me3, but mainly modulates H3K27ac status during macrophages maturation.
Project description:To study the dynamic changes of histone modifications across HSV-1 genome during lytic infection in THP-1 cells. Totally 20 maps of HSV-1 epigenome were generated at 5 different time points after infection, together with their corresponding gene expression profiles.We found that histone modifications were detected on HSV-1 genome soon after infection; all four studied modifications, H3K9me3, H3K27me3, H3K4me3 and H3K27ac, change rapidly along with virus life cycle progression.The transcription repression marks, H3K9me3 and H3K27me3, tended to decrease along with infection process, and the transcription activation mark H3K27ac increased on viral genome, which were aligned with increased expression of viral genes. Moreover, treatment with C646, an inhibitor for H3K27ac transferase p300, inhibited expression of viral genes; and EPZ6438, an inhibitor for H3K27 methyltransferase EZH2, enhanced viral gene expression.
Project description:To study the dynamic changes of histone modifications across HSV-1 genome during lytic infection in THP-1 cells. Totally 20 maps of HSV-1 epigenome were generated at 5 different time points after infection, together with their corresponding gene expression profiles.We found that histone modifications were detected on HSV-1 genome soon after infection; all four studied modifications, H3K9me3, H3K27me3, H3K4me3 and H3K27ac, change rapidly along with virus life cycle progression.The transcription repression marks, H3K9me3 and H3K27me3, tended to decrease along with infection process, and the transcription activation mark H3K27ac increased on viral genome, which were aligned with increased expression of viral genes. Moreover, treatment with C646, an inhibitor for H3K27ac transferase p300, inhibited expression of viral genes; and EPZ6438, an inhibitor for H3K27 methyltransferase EZH2, enhanced viral gene expression.
Project description:Considered as fundamental epigenetic regulators controlling many key cellular processes, histone modifications are a well-conserved and widely studied class of epigenetic modifications. Genome-wide studies have identified enhancers as DNA sequences that bind to H3K4me1 and H3K27ac and promoters as DNA sequences that bind to H3K4me3. To explore how the Twist1 complex (Twist1/YY1/p300) regulates miR-9 expression, we performed ChIP-seq in PLC-PRF-5 cells, providing a panorama of p300, H3K4me3, H3K4me1, and H3K27ac.
Project description:OCI-AML3 Acute myeloid leukemia cell line was used for ChIP-sequencing profiling of H3K4me3, H3K4me1, H3K9ac and H3K27ac histone post-translational modifications to identify active promoter and enhancer regions.