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Publication : Runx3 deficiency results in myeloproliferative disorder in aged mice.

First Author  Wang CQ Year  2013
Journal  Blood Volume  122
Issue  4 Pages  562-6
PubMed ID  23741011 Mgi Jnum  J:201784
Mgi Id  MGI:5515696 Doi  10.1182/blood-2012-10-460618
Citation  Wang CQ, et al. (2013) Runx3 deficiency results in myeloproliferative disorder in aged mice. Blood 122(4):562-6
abstractText  The RUNX family genes encode transcription factors that are involved in development and human diseases. RUNX1 is one of the most frequently mutated genes in human hematological malignancies and is a critical factor for the generation and maintenance of hematopoietic stem cells. Another Runx family gene, Runx3, is known to be expressed in hematopoietic cells. However, its involvement in hematopoiesis remains unclear. Here we show the hematopoietic phenotypes in Runx3 conditional knockout (KO) mice (Runx3(fl/fl);Mx1-Cre(+)): whereas young Runx3 KO mice did not exhibit any significant hematopoietic defects, aged Runx3 KO mice developed a myeloproliferative disorder characterized by myeloid-dominant leukocytosis, splenomegaly, and an increase of hematopoietic stem/progenitor cells (HSPCs). Notably, Runx3-deficient cells showed hypersensitivity to granulocyte-colony stimulating factor, suggesting enhanced proliferative and mobilization capability of Runx3-deficient HSPCs when stimulated. These results suggest that, besides Runx1, Runx3 also plays a role in hematopoiesis.
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