STAT5 is a critical transcription factor that is required for proper lymphocyte development. For example, STAT5 is essential for CD8 T lineage commitment, regulatory T cell (Treg) development, B cell development and lymphocyte transformation. Active phosphorylated STAT5 can bind to target genes to either activate or repress transcription, however, the mechanism by which this occurs remains unclear. We hypothesize that STAT5 represses target genes via selective interactions with co-repressors, NCOR1 and NCOR2, and induces transcription via interactions with co-activators, CREBBP and EP300. The goal of my thesis is to characterize the role of these co-repressors and co-activators in lymphocyte development (B and T cell) and transformation (B cell acute lymphoblastic leukemia).
For work prior to UMN MSTP
Pomeroy EJ, Lee LA, Lee RD, Schirm DK, Temiz NA, Ma J, Gruber TA, Diaz-Flores E, Moriarity BS, Downing JR, Shannon KM, Largaespada DA, Eckfeldt CE. Ras oncogene-independent activation of RALB signaling is a targetable mechanism of escape from NRAS(V12) oncogene addiction in acute myeloid leukemia. Oncogene. 2017 Jun 8;36(23):3263-3273. PMCID: PMC5464975
Eckfeldt CE, Pomeroy EJ, Lee RD, Hazen KS, Lee LA, Moriarity BS, Largaespada DA. RALB provides critical survival signals downstream of Ras in acute myeloid leukemia. Oncotarget. 2016 Oct 4;7(40):65147-65156. PMCID: PMC5323144
Lee RD, Song MY, Lee JK. Large-scale profiling and identification of potential regulatory mechanisms for allelic gene expression in colorectal cancer cells. Gene. 2013 Jan 1;512(1):16-22.