Figure 5
Figure 5. Knock-down of endogenous THAP1 in human primary ECs inhibits expression of pRB/E2F cell-cycle target genes RRM1, Mad2, survivin, HMMR, RRM2, CDC2, cyclin B1, and DLG7. (A,B) Expression level analysis by qPCR following siRNA-mediated knock-down of THAP1 in primary human ECs. RNA was isolated from ECs transfected with siTHAP1-1 (A), siTHAP1-3 (B), or siLuc siRNAs 48 hours after siRNA transfection, and used for qPCR analysis with the indicated human gene primers (control gene: actin; pRB/E2F cell-cycle target genes: RRM1, Mad2, survivin, HMMR, RRM2, CDC2, cyclin B1, and DLG7). NF-KB2 p100 was used as a control gene for normalization. The mean and standard error for 2 independent data sets are shown.

Knock-down of endogenous THAP1 in human primary ECs inhibits expression of pRB/E2F cell-cycle target genes RRM1, Mad2, survivin, HMMR, RRM2, CDC2, cyclin B1, and DLG7. (A,B) Expression level analysis by qPCR following siRNA-mediated knock-down of THAP1 in primary human ECs. RNA was isolated from ECs transfected with siTHAP1-1 (A), siTHAP1-3 (B), or siLuc siRNAs 48 hours after siRNA transfection, and used for qPCR analysis with the indicated human gene primers (control gene: actin; pRB/E2F cell-cycle target genes: RRM1, Mad2, survivin, HMMR, RRM2, CDC2, cyclin B1, and DLG7). NF-KB2 p100 was used as a control gene for normalization. The mean and standard error for 2 independent data sets are shown.

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