Fig. 6.
Fig. 6. Modulation of C/EBPɛ mRNA expression by retinoids in HL-60 and NB4 cells. Upper panel: cells were treated for 48 hours with 10-7 mol/L retinoid, either alone or in combination with 10-7 mol/L ATRA. Total RNA was extracted and analyzed by Northern blot technique (10 μg/lane) and hybridized with [32P]-labeled C/EBPɛ cDNA as described in Materials and Methods. The same blot was rehybridized with [32P]-labeled β-actin probe to show RNA loading in each lane; results for HL-60 and NB4 were independently normalized such that expression in wild-type cells equaled one. HL-60 cells (lanes 1 through 7) and NB4 cells (lanes 8 through 14) were cultured for 48 hours with 10-7 mol/L retinoid as follows: untreated control (lanes 1, 8); ATRA (lanes 2, 9); Retinoid C (lanes 3, 10); Retinoid D (lanes 4, 11); Retinoid E (lanes 5, 12); ATRA plus Retinoid D (lanes 6, 13); ATRA plus Retinoid E (lanes 7, 14). Lower panel: Densitometric quantitation of upper panel. Signal intensity of C/EBPɛ in untreated HL-60 cells (lane 1) and NB4 cells (lane 8) were used as the control.

Modulation of C/EBPɛ mRNA expression by retinoids in HL-60 and NB4 cells. Upper panel: cells were treated for 48 hours with 10-7 mol/L retinoid, either alone or in combination with 10-7 mol/L ATRA. Total RNA was extracted and analyzed by Northern blot technique (10 μg/lane) and hybridized with [32P]-labeled C/EBPɛ cDNA as described in Materials and Methods. The same blot was rehybridized with [32P]-labeled β-actin probe to show RNA loading in each lane; results for HL-60 and NB4 were independently normalized such that expression in wild-type cells equaled one. HL-60 cells (lanes 1 through 7) and NB4 cells (lanes 8 through 14) were cultured for 48 hours with 10-7 mol/L retinoid as follows: untreated control (lanes 1, 8); ATRA (lanes 2, 9); Retinoid C (lanes 3, 10); Retinoid D (lanes 4, 11); Retinoid E (lanes 5, 12); ATRA plus Retinoid D (lanes 6, 13); ATRA plus Retinoid E (lanes 7, 14). Lower panel: Densitometric quantitation of upper panel. Signal intensity of C/EBPɛ in untreated HL-60 cells (lane 1) and NB4 cells (lane 8) were used as the control.

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