Figure 3.
Figure 3. Specific amplification of KIRs in K562. RNA was amplified using primers specific for KIR2DL1, KIR2DL2, KIR2DL4, KIR3DL1, KIR3DL2, KIR2DS1, KIR2DS2, KIR2DS3, KIR2DS4, KIR2DS5, and KIR3DS1 from K562 cells that were untransfected (Control, lane 2), pcDNA3 vector control transfected (Vector, lane 3), pcDNA3-KIR2DS2 transfected (KIR2DS2, lane 4), and pcDNA3-KIR2DS4 transfected (KIR2DS4, lane 5). Normal 1 was used as a positive control for all KIR primers (lane 6) but was found to be negative for KIR3DL1 (D). β-Actin primers were included to ensure that a similar amount of cDNA was present in each sample (top band, β-Act). Reaction with water was included as a negative control for each set of primers (Mock, lane 1).

Specific amplification of KIRs in K562. RNA was amplified using primers specific for KIR2DL1, KIR2DL2, KIR2DL4, KIR3DL1, KIR3DL2, KIR2DS1, KIR2DS2, KIR2DS3, KIR2DS4, KIR2DS5, and KIR3DS1 from K562 cells that were untransfected (Control, lane 2), pcDNA3 vector control transfected (Vector, lane 3), pcDNA3-KIR2DS2 transfected (KIR2DS2, lane 4), and pcDNA3-KIR2DS4 transfected (KIR2DS4, lane 5). Normal 1 was used as a positive control for all KIR primers (lane 6) but was found to be negative for KIR3DL1 (D). β-Actin primers were included to ensure that a similar amount of cDNA was present in each sample (top band, β-Act). Reaction with water was included as a negative control for each set of primers (Mock, lane 1).

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