Fig. 4.
Fig. 4. Delay of granulocytic differentiation by HES-1 in 32D cells and abolishment of this phenotype by DN-GATA. / The original 32D cells were transfected with the SRα promoter-driven HES-1 cDNA and selected for G418. Some G418-resistant clones were further infected with a mock virus or a DN-GATA–containing pMX/IRES-EGFPpuro virus. The morphology of the cells 4 days after the addition of G-CSF is shown in panel A (Wright-Giemsa staining). Original magnification × 400. Three independent DN-GATA–expressing clones derived from each of 2 independent HES-1–expressing clones were investigated. (B) The ratio of undifferentiated cells after successive days of culture is shown. The results are expressed as the mean values of 3 independent experiments, with error bars showing SD.

Delay of granulocytic differentiation by HES-1 in 32D cells and abolishment of this phenotype by DN-GATA.

The original 32D cells were transfected with the SRα promoter-driven HES-1 cDNA and selected for G418. Some G418-resistant clones were further infected with a mock virus or a DN-GATA–containing pMX/IRES-EGFPpuro virus. The morphology of the cells 4 days after the addition of G-CSF is shown in panel A (Wright-Giemsa staining). Original magnification × 400. Three independent DN-GATA–expressing clones derived from each of 2 independent HES-1–expressing clones were investigated. (B) The ratio of undifferentiated cells after successive days of culture is shown. The results are expressed as the mean values of 3 independent experiments, with error bars showing SD.

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