The SKI protooncogene enhances the in vivo repopulation

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The SKI proto-oncogene enhances the in vivo repopulation of hematopoietic stem cells and causes

The SKI proto-oncogene enhances the in vivo repopulation of hematopoietic stem cells and causes myeloproliferative disease by Sofie Singbrant, Meaghan Wall, Jennifer Moody, Göran Karlsson, Alistair M. Chalk, Brian Liddicoat, Megan R. Russell, Carl R. Walkley, and Stefan Karlsson haematol Volume 99(4): 647 -655 March 31, 2014 © 2014 by Ferrata Storti Foundation

Enforced expression of SKI results in an extensive competitive advantage and increased numbers of

Enforced expression of SKI results in an extensive competitive advantage and increased numbers of phenotypic HSCs. (A–B) Donor contribution in PB in primary and secondary recipients at the indicated time points after transplantation of one representative tr. . . Sofie Singbrant et al. Haematologica 2014; 99: 647 -655 © 2014 by Ferrata Storti Foundation

Increased levels of SKI result in skewing towards myeloid differentiation at the expense of

Increased levels of SKI result in skewing towards myeloid differentiation at the expense of lymphoid development. Sofie Singbrant et al. Haematologica 2014; 99: 647 -655 © 2014 by Ferrata Storti Foundation

SKI overexpression results in impaired BM erythropoiesis and compensatory stress erythropoiesis in the spleen.

SKI overexpression results in impaired BM erythropoiesis and compensatory stress erythropoiesis in the spleen. Sofie Singbrant et al. Haematologica 2014; 99: 647 -655 © 2014 by Ferrata Storti Foundation

SKI induces a stem cell signature and activates gene expression involved in myeloid differentiation

SKI induces a stem cell signature and activates gene expression involved in myeloid differentiation and HGF signaling. Sofie Singbrant et al. Haematologica 2014; 99: 647 -655 © 2014 by Ferrata Storti Foundation

The effect of SKI on the hematopoietic system is partially dependent on HGF-signaling, but

The effect of SKI on the hematopoietic system is partially dependent on HGF-signaling, but independent of its ability to inhibit TGF-β. Sofie Singbrant et al. Haematologica 2014; 99: 647 -655 © 2014 by Ferrata Storti Foundation