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Main Profile

Full Name and Degrees: 
James A. Thomson, M.D., Ph.D.
Member Role: 
Principal Investigator
Institutional affiliation: 
University of Wisconsin
Additional links: 

Director of Regenerative Biology, Morgridge Institute for Research; Professor of Cell and Regenerative Biology (UW); Professor, Molecular, Cellular, and Developmental Biology - University of California, Santa Barbara



Hub Site: 
02-James Thomson
research focus: 

Relevant Research Description

In the early 1990s, my lab derived ES cells from an Old World monkey (the rhesus macaque) and a New World monkey (the common marmoset), work that led to derivation of human ES cells in 1998. Much of my lab’s research after that derivation was dedicated to establishing human ES cells as an accepted, practical model system. To that end, we developed defined culture conditions, methods for genetic manipulation, and approaches for the in vitro differentiation of human ES cells to key lineages of clinical importance including hematopoietic, neural, cardiac, and placental tissues. More recently, in 2007, my laboratory described the isolation of human induced pluripotent (iPS cells) cells with the basic properties of human ES cells but derived from somatic cells.

My research now focuses on understanding how a cell can maintain or change identity, how a cell chooses between self-renewal and the initial decision to differentiate, and how a differentiated cell with limited developmental potential can be reprogrammed to a pluripotent cell.

My current research interests include:

  • Examining the transcriptional networks in ES cells that mediate self-renewal and commitment to each of the basic lineages of the early embryo.
  • Mapping the epigenome of ES cells and their early-differentiated derivatives as a participant in the San Diego Epigenome Center.
  • Improving methods for generating human iPS cells, and correcting genetic defects in iPS cells generated from patients with degenerative retinal disease.
  • Developing new strategies to convert human pluripotent stem and somatic cells into hematopoietic, vascular, and cardiac progenitor cells.
  • Understanding clocking mechanisms that control developmental rates.
Recent publications: 
Chen G, Hou Z, Gulbranson D, Thomson JA. "Actin-myosin contractility is responsible for the reduced viability of dissociated human embryonic stem cells." Cell Stem Cell (2010). 7(2): 240-248. Lister R, Pelizzola M, Kida YS, Hawkins RD, Nery JR, Hon G, Antosiewicz-Bourget J, O’Malley R, Castanon R, Downes M, Yu R, Stewart R, Ren B, Thomson JA, Evans RM,Ecker JR. “Hotspots of aberrant epigenomic reprogramming in human iPS cells.” Nature, (2011): 471(7336): 68-73. Yu P, Pan G, Yu J, Thomson JA. “FGF2 sustains NANOG and switches BMP4 induced human ES cell differentiation from trophoblast to mesendoderm.” Cell Stem Cell (2011): 8(6): 326-334. Chen G, Gulbranson D, Hou Z, Bolin J, Probasco MD, Smuga-Otto K, Howden S, Diol N, Propson NE, Wagner R, Lee GO, Antosiewicz-Bourget J, Teng JMC, Thomson JA. “Chemically defined conditions for human iPS cell derivation and culture.” Nature Methods (2011): 8(5):424-9. Howden SE, Gore A, Li Zhe, Fung H, Nisler BS, Nie J, Chen G, McIntosh BE, Gulbranson DR, Diol NR, Taapken SM, Vereide DT, Montgomery KD, Zhang K, Gamm D, Thomson JA. “Genetic correction and analysis of induced pluripotent stem cells from a patient with gyrate atrophy.” Proc Natl Acad Sci USA, Epub 4 Apr (2011).
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James A. Thomson, M.D., Ph.D.

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