Colin Stewart
Colin Stewart, has been a pioneer in developing many of the techniques that are now widely used in mouse experimental genetics, in establishing protocols for deriving embryonic stem (ES) lines,
uniparental ES lines, and for the derivation of the first human ES lines.
He was instrumental in identifying the cytokine LIF as being crucial to sustaining stem cell pluripotency (Nature 1988). Subsequently he showed that LIF and its signalling pathway is critical to regulating uterine receptivity for embryo implantation in mammals (Nature 1993). He developed numerous mouse models of congenital diseases, particularly those arising from defective genomic imprinting e.g. Prader-Willi.
Over the last decade his interests have centered on the laminopathies, a heterogeneous collection of diseases all arising from mutations in the LaminA gene. He collaborated with Nicolas Lévy, in being the first to show that mutations in the LMNA gene cause progeria (Science 2003), and to make mouse models of many of the laminopathies, including progeria. He also developed the first iPSCs lines derived from patient fibroblasts in establishing an in vitro model for Progeria (HGPS). Currently, he is a founding partner of Daedalus Therapeutics that is developing new treatments to ameliorate cardiomyopathies and vascular disease.
uniparental ES lines, and for the derivation of the first human ES lines.
He was instrumental in identifying the cytokine LIF as being crucial to sustaining stem cell pluripotency (Nature 1988). Subsequently he showed that LIF and its signalling pathway is critical to regulating uterine receptivity for embryo implantation in mammals (Nature 1993). He developed numerous mouse models of congenital diseases, particularly those arising from defective genomic imprinting e.g. Prader-Willi.
Over the last decade his interests have centered on the laminopathies, a heterogeneous collection of diseases all arising from mutations in the LaminA gene. He collaborated with Nicolas Lévy, in being the first to show that mutations in the LMNA gene cause progeria (Science 2003), and to make mouse models of many of the laminopathies, including progeria. He also developed the first iPSCs lines derived from patient fibroblasts in establishing an in vitro model for Progeria (HGPS). Currently, he is a founding partner of Daedalus Therapeutics that is developing new treatments to ameliorate cardiomyopathies and vascular disease.