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Immunity. 2000 Sep;13(3):397-407.

Abnormal Stat activation, hematopoietic homeostasis, and innate immunity in c-fes-/- mice.

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1
Committee on Genetics, University of Chicago, Illinois 60637, USA.

Abstract

The c-fes protooncogene encodes a nonreceptor tyrosine kinase (Fes) implicated in cytokine receptor signal transduction, neutrophil survival, and myeloid differentiation. To determine the role of Fes in embryonic development and hematopoiesis, we engineered a null mutation of the murine c-fes locus. c-fes-/- mice are viable but not born in the expected Mendelian ratios. Live born c-fes-/- mice exhibit lymphoid/myeloid homeostasis defects, compromised innate immunity, and increased Stat activation in response to GM-CSF and IL-6 signaling. Therefore, increased cytokine responsiveness in the absence of Fes leads to abnormal myeloid proliferation and functional defects in the macrophage lineage.

PMID:
11021537
[Indexed for MEDLINE]
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