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 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: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:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.