AML1 is a key transcription factor during hematopoietic differentiation. It is fused to various cellular proteins as a result of chromosomal translocations found in myelogenous leukemia. The best-characterized fusion involving AML1 is the AML1-ETO protein that results from t (8; 21) in patients with acute myeloid leukemia. AML1 and AML1-ETO have identical N-terminal DNA binding domains but distinct C-terminal regions. The unique C-terminal regions of AML1 and AML1-ETO may regulate interactions with DNA and other transcription factors to alter the transcriptional activity of each protein. The hypothesis of this study is that AML1 and AML1-ETO not only regulate the same genes, but also a unique set of genes because of their distinct C-termini. Therefore, the goal of this proposal is to identify novel shared and distinct AML1 and AML1-ETO target genes that regulate hematopoiesis by using chromatin immunoprecipitation coupled to microarray analysis. The identification and characterization of target gene function should provide insight into how AML1 and AML1-ETO are involved in hematopoiesis and leukemogenesis. ? ? ?
Boyapati, Anita; Ren, Bing; Zhang, Dong-Er (2011) SERPINB13 is a novel RUNX1 target gene. Biochem Biophys Res Commun 411:115-20 |
Boyapati, Anita; Yan, Ming; Peterson, Luke F et al. (2007) A leukemia fusion protein attenuates the spindle checkpoint and promotes aneuploidy. Blood 109:3963-71 |
Yan, Ming; Kanbe, Eiki; Peterson, Luke F et al. (2006) A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis. Nat Med 12:945-9 |