Research

1. The role of TGF-beta superfamily signalling in cardiovascular and pulmonary development and disease
2. The mechanism underlying mammalian pluripotency and direct nuclear programming
3. The translation of pluripotent stem and progenitor cells for viable cell and gene therapies.

Our lab’s interests are concerned with understanding the cellular and genetic mechanisms that underlie cell-fate decisions during (a) the embryogenesis, maintenance and repair/regeneration of the cardiovascular and pulmonary systems and (b) direct nuclear programming of somatic cells to pluripotency and cardiovascular/pulmonary fates.

Selected References

Rana AA, Roper S, Palmer E and Smith JC. Loss of Xenopus tropicalis EMSY causes impairment of gastrulation and and upregulation of p53. N Biotechnology (in Press)

Argasinska J*, RanaAA*, Gilchrist MJ, Lachani K, Young AC and Smith JC. Loss of REEP4 causes neural and muscle degeneration during Xenopus development. International Journal of Developmental Biology53(1):37-43 (2009)

SevillaLM*, RanaAA*, WattFM and Smith JC. Kazrin regulates keratinocyte intercellular adhesion, terminal differentiation and Xenopus ectodermal integrity. Developmental Dynamics Jun;237(6):1718-25 (2008)