Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 122kb CIITA locus(HG17) Keywords: ChIP-chip
Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 16MB gene locus(HG17) Keywords: ChIP-chip
Project description:Analysis of H3ac, H4ac, STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucletide probes at 30bp intervals tiling over non-repetitive 16MB gene locus(HG17) Keywords: ChIP-chip three replicates for each marker at each state.
Project description:Analysis of STAT1 and IRF1 binding in IFNg treated and untreated HeLa cells for 6 hours was done using 50mer oligonucleotide probes at 30bp intervals tiling over non-repetitive 16MB gene locus (HG17).
Project description:Treatment with the histone deacetylase inhibitor trichostatin a (TSA) changes the radial positioning of the CFTR gene in HeLa S3 cells. The gene relocates from the nuclear periphery to the nuclear interior. In Calu-3 cells the gene is located in the nuclear interior. To identifiy potential regulatory elements for the positioning of CFTR, the histone h3 and h4 acetylation patterns of untreated and TSA-treated HeLa S3 and untreated Calu-3 cells were determined by ChIP-chip. A CTCF site close to the CFTR promoter displayed consistent histone H3 hyperacetylation in TSA treated HeLa S3 cells and Calu-3 cells. Four Agilent 4x 44K DNA-chips (DNA-Chips: REP_1 - REP_4). HeLa untreated and TSA treated: H3ac/H3pan (Cy5/Cy3): hybridized together on four sectors - 1x regular 3x dye swap; H4ac: 3 sectors, respective H3pan reference on different sectors on the same DNA-chips (labeled with the identical fluorophore). Calu-3: H3ac/h3pan: one sector each on the same DNA-chip (labeled with the identical fluorophore) H4ac/H3pan: two sectors each on the same DNA-chips (two each on two DNA-Chips, labeled with the identical fluorophore)
Project description:ENCODE ChIP-chip study using human myelogenous leukemia cell line K-562 and anti histone H3K4me2 (Abcam; ab7766); H3K4me3 (Abcam; ab8580); H3ac (Upstate; 06-599); H4ac (Upstate; 06-866); Histone H2B (Abcam: ab1790) and Histone H3 (Abcam: ab1791) antibodies. Each antibody experiment was conducted in three biological replicates, with two technical replicates performed for each biological replicate
Project description:CIITA is the master regulator of MHC II genes expression and hence the adaptive immune response. CIITA expression itself is tightly regulated by three cell type-specific promoters, pI, pIII, and by pIV, and can also be induced by IFNg in non-immune cells. While key regulatory elements have been identified within these promoters, knowledge of transcription factors regulating CIITA is incomplete. Here, we demonstrate that the telomere-binding protein and transcriptional activator ZBTB48 directly binds to both critical activating elements within CIITA pIII and is essential for its gene expression. ZBTB48 establishes open chromatin at CIITA pIII upstream of activating H3K4me3 modifications both priming CIITA transcription for IFNg-induction and ensuring constitutive expression in primary murine B cells. Hence, ZBTB48 acts as a molecular on-off-switch for B-cell-specific CIITA expression.
