Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling

Wentian Yang (), Jianguo Wang, Douglas C. Moore, Haipei Liang, Mark Dooner, Qian Wu, Richard Terek, Qian Chen, Michael G. Ehrlich, Peter J. Quesenberry and Benjamin G. Neel
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Wentian Yang: Brown University Alpert Medical School and Rhode Island Hospital
Jianguo Wang: Brown University Alpert Medical School and Rhode Island Hospital
Douglas C. Moore: Brown University Alpert Medical School and Rhode Island Hospital
Haipei Liang: Brown University Alpert Medical School and Rhode Island Hospital
Mark Dooner: Rhode Island Hospital and Brown University Alpert Medical School
Qian Wu: University of Connecticut Health Center
Richard Terek: Brown University Alpert Medical School and Rhode Island Hospital
Qian Chen: Brown University Alpert Medical School and Rhode Island Hospital
Michael G. Ehrlich: Brown University Alpert Medical School and Rhode Island Hospital
Peter J. Quesenberry: Rhode Island Hospital and Brown University Alpert Medical School
Benjamin G. Neel: Princess Margaret Cancer Center, University Health Network, University of Toronto, Toronto, Ontario M5G 1L7, Canada

Nature, 2013, vol. 499, issue 7459, 491-495

Abstract: Deletion of Ptpn11 in a newly defined mesenchymal progenitor population in the perichondral groove of Ranvier leads to metachondromatosis by increasing Indian hedgehog expression and activating hedgehog signalling, a process that can be reversed with the use of hedgehog pathway inhibitors.

Date: 2013
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DOI: 10.1038/nature12396

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