DAVID E. LEVY, PhD

David E LevyProfessor of Pathology and Microbiology
PhD, 1985 Caltech

NYU School of Medicine
550 1st Ave MSB-548
New York NY 10016 USA
Tel: (212) 263-8192
Fax: (509) 757-3029
E-mail: david.levy@nyumc.org
Lab Website: http://pathology.med.nyu.edu/people/faculty/levy-david-e

Research Theme(s): Interaction of signal transduction, transcriptional regulation, and metabolism in the growth and differentiation of stem cells.
Keywords: JAK-STAT signaling, cell differentiation, cancer

Research Summary:

We are investigating several stem cell-related projects. The first project involves investigation of the molecular mechanisms underlying trophoblast stem (TS) cell proliferation and differentiation and the development of the mammalian placenta. We have found that absence of STAT3 leads to mouse embryonic lethality due to placental failure, the result of inadequate differentiation and survival of critical placental components. In this project, we are elucidating the role of STAT3 during TS cell lineage commitment and differentiation. One aim is to determine how STAT3 maintains TS cell character, in particular, by elucidating its downstream targets. We are also characterizing the specific STAT3 biochemical functions required for placental development.

A second stem cell project explores the commitment of hematopoietic stem cells to myeloid and plasmacytoid dendritic cell differentiation and the role of these cells during innate immunity. We are exploiting methods for conditionally immortalizing lineage committed hematopoietic progenitors that retain the capacity for terminal differentiation. We are using these systems to explore the genes and signaling pathways required for lineage commitment and differentiation and to identify genes required for specific aspects of innate immunity.

A third stem cell project explores the biology of myeloid leukemia-inducing cells following transformation by the Ras oncogene. We have found that Ras transformation requires a mitochondrial function of STAT3 that modulates cellular metabolism. Mice lacking STAT3 or expressing mutant forms of STAT3 in hematopoietic stem cells are protected from cancer development. We are exploring the biochemical basis for STAT3 action during leukemic transformation of hematopoietic stem cells.

Selected Publications: