Figure 6.
The Δ319 mutant abrogates proliferative signaling by the WT G-CSFR. BaF3 cells transfected with the WT G-CSFR (WT), Δ319 G-CSFR, or both receptor forms (WT/Δ319) were grown in G-CSF–containing media (10 ng/mL) for the indicated times. Results with 4 independent Δ319 clones with varying levels of expression of the mutant receptor are shown. (Left) Growth curve of transfectants; (Right, upper panel) WCLs from cells transfected with both the WT G-CSFR and the indicated Δ319 G-CSFR mutant clones shown in panel A were immunoblotted with anti–G-CSFR antibody (sc9173). (Right, lower panel) The blot in the upper panel was stripped and reblotted with anti-actin antibody to control for protein loading.

The Δ319 mutant abrogates proliferative signaling by the WT G-CSFR. BaF3 cells transfected with the WT G-CSFR (WT), Δ319 G-CSFR, or both receptor forms (WT/Δ319) were grown in G-CSF–containing media (10 ng/mL) for the indicated times. Results with 4 independent Δ319 clones with varying levels of expression of the mutant receptor are shown. (Left) Growth curve of transfectants; (Right, upper panel) WCLs from cells transfected with both the WT G-CSFR and the indicated Δ319 G-CSFR mutant clones shown in panel A were immunoblotted with anti–G-CSFR antibody (sc9173). (Right, lower panel) The blot in the upper panel was stripped and reblotted with anti-actin antibody to control for protein loading.

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