. Author manuscript; available in PMC: 2017 Feb 20.

Published in final edited form as: Nature. 2016 Oct 26;539(7628):304–308. doi: 10.1038/nature20131

Table 1.

Ptpn11^E76K/+ mutation in MSPCs and osteoprogenitors, but not differentiated osteoblasts or endothelial cells, in the BM microenvironment induces MPN

Cell-type-specific knock-in mice	Target cells	Age of mice euthanized	Incidence of MPN	HSC hyperactivation	Spleen weight (g)
Ptpn11^E76K/+Nestin-Cre⁺	MSPCs	7–14 months	20/27***	Yes	0.289 ± 0.054
Ptpn11^E76K/+VE-Cadherin-Cre⁺-ER^T2	Endothelial cells	11–18 months	0/15	No	0.098 ± 0.056
Ptpn11^E76K/+Prx1-Cre⁺	Mesenchymal cells	5–10 months	12/16***	Yes	0.385 ± 0.177
Ptpn11^E76K/+Lepr-Cre⁺	Leptin receptor⁺ mesenchymal cells	13–17 months	9/15***	Yes	0.281 ± 0.075
Ptpn11^E76K/+Osx1-Cre⁺	Osteoprogenitors	5–8 months	13/14***	Yes	0.616 ± 0.08
Ptpn11^E76K/+Oc-Cre⁺	Osteoblasts	11–18 months	0/16	No	0.109 ± 0.034

Cell-type-specific Ptpn11^E76K knock-in mice as indicated were generated and monitored for MPN development for up to 18 months. The incidence of MPN, cycling status of BM HSCs, and spleen weights of the animals euthanized at the indicated ages were determined.