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. Author manuscript; available in PMC: 2015 Jul 1.
Published in final edited form as: Genes Immun. 2014 Nov 20;16(1):89–98. doi: 10.1038/gene.2014.65

Figure 2.

Figure 2

MIR181A1B1 and MIR181A2B2 are regulated independently. A. Differential regulation in NK cells and T cells. RNA was assayed by RT-qPCR and quantification cycle (Cq) values were corrected with those of 18S rRNA or GAPDH, as described in Materials and Methods. The two RT-qPCR methods produced essentially identical relative amounts. Corrected Cq values were compared by t-test: pri-miR-181ab-1 vs. pri-miR-181ab-2 for NK cells (*, p < 0.03); T vs. NK cell for pri-miR-181ab-2 (‡, t < 0.02).The pri-miR-181ab-1/-2 ratio was significantly different in T cells vs. NK cells (t < 0.02). For graphic presentation, corrected Cq values were converted to numerical values and normalized to the level of T cell pri-miR-181ab-2. Avg and SEMs of 3 donors are presented. B. Differential regulation during NK cell development. Umbilical cord blood lymphocytes were sorted into Stages II-IV and adult blood lymphocytes were sorted into CD56bright, CD56dimCD94hi, and CD56dimCD94low subsets. RNA was extracted and analyzed for pri-miR-181ab-1 and pri-miR-181ab-2 levels by RT-qPCR. Shown are Avg and SEM pri-mir-181 RNA levels relative to GAPDH RNA. All values were multiplied by 10 000 for display purposes. * p < 0.05, † p < 0.01 for pri-miR-181ab-1 vs. pri-miR-181ab-2 differences.