Michael Kyba, PhD
Zoology, University of British Columbia, Vancouver, Canada
312 Church St SE
Minneapolis, MN 55455
MMC 508 Mayo
8508C (Campus Delivery Code)
420 Delaware St SE
Minneapolis, MN 55455
Dr. Kyba is an Assistant Professor of Pediatrics in the Division of Blood and Marrow Transplantation. He is also a member of the Lillehei Heart Institute, and an affiliate member of the Stem Cell Institute.
Dr. Kyba received his PhD degree from the University of British Columbia in 1998, and completed a postdoctoral fellowship in stem cell biology at the Whitehead Institute at MIT, Cambridge, MA in 2003. From 2003-2008, he was Assistant Professor of Developmental Biology at the University of Texas Southwestern Medical Center at Dallas, TX. He joined the faculty at the University of Minnesota in July 2008.
Dr. Kyba has published 35 research manuscripts in scientific journals, including: Cell, Science, and Nature Medicine.
Deriving therapeutic hematopoietic stem cells from embryonic stem cells.
ES cells are totipotent and capable of recapitulating all of the developmental events of embryogenesis. They are therefore theoretically the ideal source of cells for regenerative therapies. However, turning theory into practice is not straightforward, and very few successful models of such therapy exist. We have developed one successful model, based on regulated expression of members of the Hox family of transcription factors. Current work is focused on understanding how Hox genes regulate hematopoietic stem cell self-renewal and identifying regulatory circuits under Hox control.
Skeletal muscle stem cells and FSH muscular dystrophy
Certain degenerative diseases may be the result of ineffective self-renewal or differentiation of lineage specific stem cells. We are particularly interested in Fascioscapulohumeral Muscular Dystrophy (FSHD), a dominant dystrophy associated with a contraction of 4q subtelomeric repeats. Although the condition is almost certainly caused by derepression of a gene in the vicinity of 4q, the protein products of candidate genes in this area can not be detected overexpressed in patient muscle samples. Because muscle stem cells (satellite cells) are rare, proteins overexpressed specifically in satellite cells are unlikely to be identified in patient biopsies. We are testing the hypothesis that a Hox gene embedded within the 4q repeats, DUX4, causes FSHD when derepressed in muscle satellite cells.
2006 Basil O’Connor Award (March of Dimes)