Fig. 2.
Fig. 2. Binding of the PE-labeled myeloid growth factors G- and GM-CSF to cultured PU.1 null cells was minimal. Cells were prepared directly from liver of control and PU.1 null neonatal mice and cultured in the presence of IL-3, GM-CSF, and G-CSF for 9 days to expand populations of Gr-1+ cells. Wild-type and PU.1 deficient cells were harvested, live cells enriched over a density gradient and then analyzed for the presence of receptors for G-CSF (G-CSFR), and for GM-CSF (GM-CSFR) by the binding of PE-conjugated G-CSF or GM-CSF (A) or for the neutrophil specific marker Gr-1 (B). (A) PE-control staining (—); PE-conjugated G-CSF or GM-CSF binding (- - -). (B) Irrelevant control antibody staining (—); specific anti-Gr-1 antibody staining (- - -).

Binding of the PE-labeled myeloid growth factors G- and GM-CSF to cultured PU.1 null cells was minimal. Cells were prepared directly from liver of control and PU.1 null neonatal mice and cultured in the presence of IL-3, GM-CSF, and G-CSF for 9 days to expand populations of Gr-1+ cells. Wild-type and PU.1 deficient cells were harvested, live cells enriched over a density gradient and then analyzed for the presence of receptors for G-CSF (G-CSFR), and for GM-CSF (GM-CSFR) by the binding of PE-conjugated G-CSF or GM-CSF (A) or for the neutrophil specific marker Gr-1 (B). (A) PE-control staining (—); PE-conjugated G-CSF or GM-CSF binding (- - -). (B) Irrelevant control antibody staining (—); specific anti-Gr-1 antibody staining (- - -).

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