Fig. 1.
Fig. 1. Activation by GM-CSF of Stat1α and Stat3 and suppression by GM-CSF of EPO-induced erythroid differentiation. (A) UT-7/GM cells were cultured with GM-CSF (10 ng/mL) and/or EPO (10 U/mL). Seven days later, cells were harvested for dianisidine staining. The data are the means ± standard deviation (SD) of triplicate cultures. (B) Growth factor-starved UT-7/GM cells were treated with EPO (10 U/mL) and/or GM-CSF (10 ng/mL) for 15 minutes. Nuclear extracts were then prepared for an EMSA with32P-labeled SIE or β-CAP probes. Arrows A, B, and C indicate a homodimer of Stat3, a heterodimer of Stat1α and Stat3, and a homodimer of Stat1α, respectively (see Kirito et al13and text).

Activation by GM-CSF of Stat1α and Stat3 and suppression by GM-CSF of EPO-induced erythroid differentiation. (A) UT-7/GM cells were cultured with GM-CSF (10 ng/mL) and/or EPO (10 U/mL). Seven days later, cells were harvested for dianisidine staining. The data are the means ± standard deviation (SD) of triplicate cultures. (B) Growth factor-starved UT-7/GM cells were treated with EPO (10 U/mL) and/or GM-CSF (10 ng/mL) for 15 minutes. Nuclear extracts were then prepared for an EMSA with32P-labeled SIE or β-CAP probes. Arrows A, B, and C indicate a homodimer of Stat3, a heterodimer of Stat1α and Stat3, and a homodimer of Stat1α, respectively (see Kirito et al13and text).

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