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JCI table of contents: Dec. 3, 2007
Date:12/3/2007

t lack the protein Gata-1, rendering them incapable of further differentiation. When G1ME cells were engineered to produce STAT1, a protein that is expressed in response to inflammatory markers, they displayed distinguishing characteristics of megakaryocytic differentiation, including the expression of genes found in platelets and chromosomal duplication. Similarly, megakaryocytes from mice deficient in STAT1 lacked the chromosomal duplication inherent to this cell type. The authors concluded from these results that inflammatory stimulation of STAT1 can lead to thrombocytosis through enhanced differentiation of platelet precursor cells.

TITLE: STAT1 promotes megakaryopoiesis downstream of GATA-1 in mice

AUTHOR CONTACT:
John D. Crispino
Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Phone: (312) 503-1504; Fax: (312) 503-0189; E-mail: j-crispino@northwestern.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33010


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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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