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Items: 3

1.

RUNX1-ETO orchestrates dynamic enhancer promoter communication in t(8;21) Acute Myeloid Leukaemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: WIG
Series
Accession:
GSE121282
ID:
200121282
2.

RUNX1-ETO orchestrates dynamic enhancer promoter communication in t(8;21) Acute Myeloid Leukaemia (DNaseI-Seq)

(Submitter supplied) Acute myeloid leukaemia (AML) is caused by mutations in transcriptional and epigenetic regulator genes impairing myeloid differentiation. The t(8;21)(q22;q22) translocation generates the leukemogenic RUNX1-ETO fusion protein which interferes with the hematopoietic master regulator RUNX1. We previously showed that maintenance of t(8;21) AML is dependent on RUNX1-ETO as its depletion causes extensive changes in transcription factor binding and gene expression as well as myeloid differentiation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: WIG
Series
Accession:
GSE121281
ID:
200121281
3.

RUNX1-ETO orchestrates dynamic enhancer promoter communication in t(8;21) Acute Myeloid Leukaemia (ChIP-Seq)

(Submitter supplied) Acute myeloid leukaemia (AML) is caused by mutations in transcriptional and epigenetic regulator genes impairing myeloid differentiation. The t(8;21)(q22;q22) translocation generates the leukemogenic RUNX1-ETO fusion protein which interferes with the hematopoietic master regulator RUNX1. We previously showed that maintenance of t(8;21) AML is dependent on RUNX1-ETO as its depletion causes extensive changes in transcription factor binding and gene expression as well as myeloid differentiation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: WIG
Series
Accession:
GSE121280
ID:
200121280
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