Abstract:
:To investigate the specificity of cytokine signals in hematopoietic differentiation, we generated mice with a targeted mutation of their G-CSF receptor (G-CSFR) such that the cytoplasmic (signaling) domain of the G-CSFR is replaced with the cytoplasmic domain of the erythropoietin receptor. In homozygous mutant mice, expression of this chimeric receptor had no apparent affect on lineage commitment and was able to support the production of morphologically mature neutrophils. However, mutant neutrophils displayed reduced chemotaxis, and G-CSF-stimulated mobilization of neutrophils and hematopoietic progenitors from the bone marrow to blood was markedly impaired. Thus, the G-CSFR is generating unique signals that are required for certain specialized hematopoietic cell functions but are not required for granulocytic differentiation or lineage commitment.
journal_name
Immunityjournal_title
Immunityauthors
Semerad CL,Poursine-Laurent J,Liu F,Link DCdoi
10.1016/s1074-7613(00)80090-4keywords:
subject
Has Abstractpub_date
1999-08-01 00:00:00pages
153-61issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(00)80090-4journal_volume
11pub_type
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