@article{SCI6160,
author = {Jie Wu},
title = {Shp2 regulates leukemic stem cell frequency in MLL-rearranged acute myeloid leukemia},
journal = {Stem Cell Investigation},
volume = {2},
number = {4},
year = {2015},
keywords = {},
abstract = {Shp2 is a non-receptor protein tyrosine phosphatase (PTP) encoded by the PTPN11 gene. It contains two SH2 domains, a PTP domain, and a carboxyl-terminal region with tyrosine phosphorylation sites. The Shp2 PTP activity is autoinhibited by its N-SH2 domain. Shp2 is activated by docking to specific tyrosine phosphorylated sites via SH2 domains or by gain-of-function (GOF) mutations that disrupt the autoinhibition. GOF Shp2 mutations are most frequently detected in juvenile myelomonocytic leukemia (JMML), representing 35% of cases. Animal model studies using conditional knockin of GOF Shp2E76K or Shp2D61G in the hematopoietic compartments have shown that these Shp2 mutants cause JMML-like myeloproliferative disease (MPD), albeit after ~6 months of latency (1,2).},
issn = {2313-0792}, url = {https://sci.amegroups.org/article/view/6160}
}