| Dataset ID | Technology | Samples |
|---|---|---|
| EGAD00001006555 | Illumina HiSeq 2500,NextSeq 500 | 91 |
Dataset Description
To investigate the mechanism by which GATA1s and STAG2 deficiency contribute to Down Syndrome leukemogenesis, specifically within the propagating CD34/CD117 cell fractions from primary xenografts, we carried out transcriptional and epigenetic profiling by RNAseq and ATACseq. The chromatin accessibility landscape was compared to bulk ATACseq of
individually sorted N-FL HSPC subpopulations.
To investigate the mechanism underlying the synergy between T21 and GATA1s in driving preleukemia development, we analyzed the binding occupancy of GATA1. We performed Cut&Run assays to profile
genome-wide GATA1 binding sites and also to quantify binding changes upon GATA1s editing in N-FL and T21-FL CD34+ enriched HSPCs. Lastly, we profiled miRNAs from N-FL and T21-FL CD34+ enriched
HSPCs by miRNA-Seq.
individually sorted N-FL HSPC subpopulations.
To investigate the mechanism underlying the synergy between T21 and GATA1s in driving preleukemia development, we analyzed the binding occupancy of GATA1. We performed Cut&Run assays to profile
genome-wide GATA1 binding sites and also to quantify binding changes upon GATA1s editing in N-FL and T21-FL CD34+ enriched HSPCs. Lastly, we profiled miRNAs from N-FL and T21-FL CD34+ enriched
HSPCs by miRNA-Seq.
Who controls access to this dataset
For each dataset that requires controlled access, there is a corresponding Data Access Committee (DAC) who determine access permissions. Access to actual data files is not managed by the EGA. If you need to request access to this data set, please contact:
Placeholder DAC
Contact person: Natalie Stickle
Email: natalie [dot] stickle [at] uhn [dot] ca
More details: EGAC00001001788
