Gary Felsenfeld Professor of Cell and Regenerative Biology; Director, UW-Madison Blood Research Program
Phone: (608) 265-6446
RESEARCH INTERESTS - Hematopoiesis, Stem and Progenitor Cell Biology, and Genomics/Epigenomics: Fundamental and Translational Science
B.S., 1984, University of Vermont, Burlington, VT, Biochemistry (honors)
B.A., 1984, University of Vermont, Burlington, VT, Anthropology
Ph.D., 1989, University of Michigan, Ann Arbor, MI, Pharmacology (with William B. Pratt)
We use multidisciplinary approaches to understand how stem and progenitor cells form the diverse complement of blood cells under normal and pathological conditions. In addition, we study the regulation of genes and chromosomes (including epigenetics), and developmental/function of the vascular biology. Our team has expertise in genomics, proteomics, chemical genetics, and computational analysis, as well as powerful molecular, cellular and biochemical technologies.
A major effort involves discovering and deciphering genetic networks that regulate the genesis and function of hematopoietic stem and progenitor cells. This program encompasses basic and translational/clinical science. Defining such mechanisms has enormous importance, as their disruption leads to adult and pediatric blood cell pathologies (leukemia, lymphoma, myelodysplastic syndrome, anemia and immunodeficiency). While hematopoietic stem cells are routinely transplanted to treat diverse diseases, their critical long-term repopulating activity is poorly understood and cannot be readily modulated for therapeutic application. Mechanistic insights can be exploited to develop novel approaches to therapeutically modulate hematopoietic stem cells, hematopoiesis, and blood cell malignancies.
Another program focuses on the mechanisms governing the normal development/function of red blood cells and regeneration of the hematopoietic compartment in the context of stress associated with conditions such as chronic infection and aging. Goals of this work include discovering novel mechanisms, developing translational strategies, and advancing fundamental knowledge in broadly important areas of biomedical science.
Since GATA-2 controls the emergence of hematopoietic stem cells from hemogenic endothelium, angiogenesis, vascular integrity, and developmental of the lymphatic system, we are studying how GATA-2 functions in the vascular system in normal and pathological states, including cancer.
Dr. Bresnick and his team are passionate about making biological and mechanistic discoveries, translating discoveries into clinical insights and strategies, and training the next-generation of multidisciplinary researchers/scholars (undergraduates, graduate students, postdoctoral fellows). Interested candidates can apply to email@example.com .
- Katsumura KR, Bresnick EH, GATA Factor Mechanisms Group. (2017) The GATA factor revolution in hematology. Blood. 2017 Apr 13;129(15):2092-2102. Review.
- Mehta C, Johnson KD, Gao X, Ong IM, Katsumura KR, McIver SC, Ranheim EA, Bresnick EH. (2017) Integrating Enhancer Mechanisms to Establish a Hierarchical Blood Development Program. Cell Rep. Sep 19;20(12):2966-2979
- Katsumura KR, Ong IM, DeVilbiss AW, Sanalkumar R, Bresnick EH.(2016) GATA Factor-Dependent Positive-Feedback Circuit in Acute Myeloid Leukemia Cells. Cell Rep. Aug 30;16(9):2428-41.
- McIver SC, Katsumura KR, Davids E, Liu P, Kang YA, Yang D, Bresnick EH. (2016) Exosome complex orchestrates developmental signaling to balance proliferation and differentiation during erythropoiesis. Elife. Aug 20;5.
- Hewitt KJ, Katsumura KR, Matson DR, Devadas P, Tanimura N, Hebert AS, Coon JJ, Kim JS, Dewey CN, Keles S, Hao S, Paulson RF, Bresnick EH. (2017) GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia. Dev Cell. Aug 7;42(3):213-225.e4.
- Hewitt KJ, Kim DH, Devadas P, Prathibha R, Zuo C, Sanalkumar R, Johnson KD, Kang YA, Kim JS, Dewey CN, Keles S, Bresnick EH. (2015) Hematopoietic Signaling Mechanism Revealed from a Stem/Progenitor Cell Cistrome. Mol Cell. 2015 Jul 2;59(1):62-74