Project description:CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets. To identify Runx3 regulated genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of CD8+ T cells were separately obtained from individual mice, TCR activated and cultured for 4 days with IL-2.
Project description:ChIP-seq was conducted using FACS-isolated CD11chiMHCII+CD4+ splenic WT DC and anti-Runx3 antibodies (Ab). Two biological Runx3 IP repeats and two input controls from sorted CD4 DC
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT CD8+ T cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads, collected from 18 WT mice.
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT NK cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Runx3 and H3K4me1 IP from splenic NK cells isolated by negative selection using NK cell isolation kit (R&D) followed by sorting of NKp46+ cells.
Project description:ChIP-seq was conducted on isolated splenic WT CD8+ T cells, TCR-activated and cultured with IL-2 using anti-Runx3 antibodies (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from TCR-activated and IL-2 cultured splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads.
Project description:ChIP-seq was conducted using splenic WT NK cells cultured for 7 days with IL-2 using anti-Runx3 antibodies (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3, one H3K4me1 and two NIS IP repeats from splenic NK cells isolated from individual mice by negative selection using NK cell isolation kit (R&D) cultured with IL-2.
Project description:ChIP-seq was conducted using freshly isolated splenic WT NK cells from IL-15/Ra treated mice with anti-Runx3 antibody (Ab) and non-immune serum (NIS) as control. Runx3 and NIS IP from splenic NK cells of IL-15/Ra treated WT mice, isolated by negative selection using NK cell isolation kit (R&D) followed by sorting of NKp46+ cells.
Project description:CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets. To identify Runx3 responsive genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of freshly isolated CD8+ T cells (resting) were separately obtained from individual mice.
Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA
Project description:We performed ChIP-Seq for 5 different transcription factors (Pol II, JunD, cFos, Max and cMyc) as part of the ENCODE project in order to determine sites of allele-specific binding. This was done in the GM12878 cell line which was genotyped as part of the pilot II phase of the 1000 genomes project. There is a matching RNA-Seq experiemnt performed on the same cell line. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Mapping TF binding sites for 5 different TFs to assess allele-specific binding