To this end we determined dynamic alterations of histone acetylation, RNA Polymerase II binding and RUNX1 occupancy in the presence or absence of RUNX1/ETO using a knockdown approach. To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8 21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The t(8 21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. Genome binding/occupancy profiling by high throughput sequencing GEO help: Mouse over screen elements for information.ĭepletion of RUNX1/ETO in t(8 21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding
0 kommentar(er)
