Fig. 8.
Fig. 8. The half-life of the c-kit transcript is not reduced by the stroma cell interaction. The reduction of the c-kit mRNA level was monitored after actinomycin D inhibition (5.0 μg/mL) of RNA synthesis in TF-1 cells. Only data of the first 4 hours of inhibition were evaluated, because the cells tended to clump under prolonged action of actinomycin D. The decrease of c-kit mRNA was measured by semiquantitative RT-PCR. One-fifth dilutions of the RNA were reverse transcribed and amplified to check linearity of amplification. These amplification products correspond to the second lane at each time point. Amplification of c-kit–specific transcripts in TF-1 cells and c-myc–specific transcripts was performed for 18 cycles. Amplification of c-kit specific transcripts was performed for 22 cycles in case of the TF-1S #MB8 cells.

The half-life of the c-kit transcript is not reduced by the stroma cell interaction. The reduction of the c-kit mRNA level was monitored after actinomycin D inhibition (5.0 μg/mL) of RNA synthesis in TF-1 cells. Only data of the first 4 hours of inhibition were evaluated, because the cells tended to clump under prolonged action of actinomycin D. The decrease of c-kit mRNA was measured by semiquantitative RT-PCR. One-fifth dilutions of the RNA were reverse transcribed and amplified to check linearity of amplification. These amplification products correspond to the second lane at each time point. Amplification of c-kit–specific transcripts in TF-1 cells and c-myc–specific transcripts was performed for 18 cycles. Amplification of c-kit specific transcripts was performed for 22 cycles in case of the TF-1S #MB8 cells.

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