| First Author | Hackenmiller R | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 3 | Pages | 397-407 |
| PubMed ID | 11021537 | Mgi Jnum | J:64748 |
| Mgi Id | MGI:1889938 | Doi | 10.1016/s1074-7613(00)00039-x |
| Citation | Hackenmiller R, et al. (2000) Abnormal Stat activation, hematopoietic homeostasis, and innate immunity in c-fes-/- mice. Immunity 13(3):397-407 |
| abstractText | 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. |
