Fig. 1.
Fig. 1. Bcr-Abl inhibition of G-CSF–induced granulocytic differentiation in 32Dcl3 cells by a kinase-dependent mechanism. / (A) Abl (top panel) and phosphotyrosine (bottom panel) immunoblots of lysates from either 32Dcl3, 32DBcr-Ablwt or 32DBcr-AblK1172R cells. (B) Morphological differentiation of 32Dcl3, 32DBcr-Ablwt, or 32DBcr-AblK1172R cells 8 days after stimulation with G-CSF as assessed by May-Gruenwald-Giemsa staining (original magnification, × 400). Cells grown in the presence of IL-3 are shown as a control. (C) Expression of Gr-1 on 32Dcl3, 32DBcr-Ablwt, or 32DBcr-AblK1172R cells upon G-CSF stimulation. Gr-1 expression on cells grown in the presence of IL-3 is shown as a control.

Bcr-Abl inhibition of G-CSF–induced granulocytic differentiation in 32Dcl3 cells by a kinase-dependent mechanism.

(A) Abl (top panel) and phosphotyrosine (bottom panel) immunoblots of lysates from either 32Dcl3, 32DBcr-Ablwt or 32DBcr-AblK1172R cells. (B) Morphological differentiation of 32Dcl3, 32DBcr-Ablwt, or 32DBcr-AblK1172R cells 8 days after stimulation with G-CSF as assessed by May-Gruenwald-Giemsa staining (original magnification, × 400). Cells grown in the presence of IL-3 are shown as a control. (C) Expression of Gr-1 on 32Dcl3, 32DBcr-Ablwt, or 32DBcr-AblK1172R cells upon G-CSF stimulation. Gr-1 expression on cells grown in the presence of IL-3 is shown as a control.

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