Figure 2.
Figure 2. Effect of Gfi-1B knock-down by a RNAi strategy. (A) Antisense (left) or siRNA (right) Eg5 were electroporated in K562 cells. Percent of cells in G2/M phases of the cell cycle was determined 48 hours after electroporation. (B) A fluorescein-labeled nonrelevant siRNA was electroporated in K562 cells, and the percent of fluorescent cells was measured before (left) and the day after electroporation (right). (C) Gfi-1B expression determined by Northern blot analysis. The Gfi-1B–specific siRNA or the sense strand alone were electroporated in K562 cells, and Gfi-1B expression level was measured 7, 20, and 48 hours after electroporation. Ribosomal 18S RNA was used as control of RNA deposit. (D) siRNA delays AraC induced hemoglobinization of K562 cells. K562 cells were electroporated without (buffer, ♦) or with sense (▴), antisense (•), or siRNA (▪) and immediately exposed to aracytine. Benzidine staining was monitored each day.

Effect of Gfi-1B knock-down by a RNAi strategy. (A) Antisense (left) or siRNA (right) Eg5 were electroporated in K562 cells. Percent of cells in G2/M phases of the cell cycle was determined 48 hours after electroporation. (B) A fluorescein-labeled nonrelevant siRNA was electroporated in K562 cells, and the percent of fluorescent cells was measured before (left) and the day after electroporation (right). (C) Gfi-1B expression determined by Northern blot analysis. The Gfi-1B–specific siRNA or the sense strand alone were electroporated in K562 cells, and Gfi-1B expression level was measured 7, 20, and 48 hours after electroporation. Ribosomal 18S RNA was used as control of RNA deposit. (D) siRNA delays AraC induced hemoglobinization of K562 cells. K562 cells were electroporated without (buffer, ♦) or with sense (▴), antisense (•), or siRNA (▪) and immediately exposed to aracytine. Benzidine staining was monitored each day.

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