Figure 2
Figure 2. DPY30 KD impaired myelomonocytic differentiation of human HPCs. Control and DPY30-KD human CD34+ cells were cultured with appropriate cytokine conditions that permit myelomonocytic differentiation. (A) Cell morphology at day 11 under such culture condition. (B) Percentage of myelomonocytic population (CD34−CD11b+) at day 14 in the differentiation assays were quantified. Averages ± SD from 3 biological repeats (infections) are plotted. **P < .01 (Student t test). (C) RNAs from the control and DPY30-KD (by short hairpin [sh]#2) cells on day 9 during myelomonocytic differentiation were subject to microarray assays followed by gene ontology analysis for the genes downregulated over twofold by DPY30 KD (listed in supplemental Table 4). (D) RNAs from the control and DPY30-KD (by sh#2 and #5) cells at day 0 (d0) and day 14 (d14) during myelomonocytic differentiation were subject to quantitative reverse-transcription polymerase chain reaction for selected genes highlighted in supplemental Table 4. Averages ± SD from 2 independent biological repeats are plotted.

DPY30 KD impaired myelomonocytic differentiation of human HPCs. Control and DPY30-KD human CD34+ cells were cultured with appropriate cytokine conditions that permit myelomonocytic differentiation. (A) Cell morphology at day 11 under such culture condition. (B) Percentage of myelomonocytic population (CD34CD11b+) at day 14 in the differentiation assays were quantified. Averages ± SD from 3 biological repeats (infections) are plotted. **P < .01 (Student t test). (C) RNAs from the control and DPY30-KD (by short hairpin [sh]#2) cells on day 9 during myelomonocytic differentiation were subject to microarray assays followed by gene ontology analysis for the genes downregulated over twofold by DPY30 KD (listed in supplemental Table 4). (D) RNAs from the control and DPY30-KD (by sh#2 and #5) cells at day 0 (d0) and day 14 (d14) during myelomonocytic differentiation were subject to quantitative reverse-transcription polymerase chain reaction for selected genes highlighted in supplemental Table 4. Averages ± SD from 2 independent biological repeats are plotted.

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