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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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STAT-3 activation is required for normal G-CSF-dependent proliferation and granulocytic differentiation.

To investigate the role of signal transducer and activator of transcription (STAT) proteins in granulocyte colony-stimulating factor (G-CSF)-regulated biological responses, we generated transgenic mice with a targeted mutation of their G-CSF receptor (termed d715F) that abolishes G-CSF-dependent STAT-3 activation and attenuates STAT-5 activation. Homozygous mutant mice are severely neutropenic with an accumulation of immature myeloid precursors in their bone marrow. G-CSF-induced proliferation and granulocytic differentiation of hematopoietic progenitors is severely impaired. Expression of a constitutively active form of STAT-3 in d715F progenitors nearly completely rescued these defects. Conversely, expression of a dominant-negative form of STAT-3 in wild-type progenitors results in impaired G-CSF-induced proliferation and differentiation. These data suggest that STAT-3 activation by the G-CSFR is critical for the transduction of normal proliferative signals and contributes to differentiative signals.[1]

References

  1. STAT-3 activation is required for normal G-CSF-dependent proliferation and granulocytic differentiation. McLemore, M.L., Grewal, S., Liu, F., Archambault, A., Poursine-Laurent, J., Haug, J., Link, D.C. Immunity (2001) [Pubmed]
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