The AML-1B gene product has been implicated in numerous translocations leading to leukemia. AML-1B is a transcription factor shown to be involved in hematopoietic differentiation. Our preliminary results show that over expressing wild-type AML-1B shortens the G1 phase of the cell cycle. The goals of this research are to identify the pathway(s) by which AML-1B affects cell cycle progression. We will use DNA microarray technology to ask what are the transcriptional targets of AML-1B, what pathways the targets feed into, and which targets are involved in the cell cycle phenotype observed for AML-1B. We will take advantage of the fact that AML-lB belongs to a family of transcription factors that all bind to the same enhancer motif. Yet out of this family, only AML-1B affects cell cycle progression. Therefore, by comparing transcriptional targets of AML-1B with one of its family members (AML-3) we should be able to eliminate numerous targets that are not likely to be involved in the cell cycle phenotype. This should increase the probability of successfully identifying targets of AML-1B which affect cell cycle progression. Thus leading the way for the identification of how the first transcription factor shown to shorten the G1 phase of the cell cycle accomplishes this feat.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Academic Research Enhancement Awards (AREA) (R15)
Project #
1R15CA091863-01
Application #
6357764
Study Section
Cell Development and Function Integrated Review Group (CDF)
Program Officer
Mufson, R Allan
Project Start
2001-08-01
Project End
2003-06-01
Budget Start
2001-08-01
Budget End
2003-06-01
Support Year
1
Fiscal Year
2001
Total Cost
$70,114
Indirect Cost
Name
University of South Carolina at Columbia
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
111310249
City
Columbia
State
SC
Country
United States
Zip Code
29208