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. 2022 Apr 20;119(17):e2110557119. doi: 10.1073/pnas.2110557119

Fig. 1.

Fig. 1.

Construction of the transgenic Cdk9 shRNA mouse model. (A) Schematic of plasmid constructs and generation of the CAGs-rtTA3/+; TG-Ren.713E (neutral control), CAGs-rtTA3/+; TG-Cdk9.421E, and CAGs-rtTA3/+; TG-Cdk9.1260E mouse strains. (B) Western blot analyses of CDK9 and RNA Pol II pSer2 inhibitions for 60 h of Dox treatment in ES cell clones containing TRE-GFP-miRE Ren.713E or two Cdk9 miRE shRNAs (Cdk9.421E and Cdk9.1260E). (C and D) Systemic expression of GFP in organs and tissues and the hematological system from CAGs-rtTA3/+; TRE-GFP-miRE Cdk9.421E mice, maintained on a Dox diet for 72 h. (E) Quantitative RT-PCR of Cdk9 in multiple organs from “1”: CAGs-rtTA3/+; TG-Ren.713E and “2”: CAGs-rtTA3/+; TG-Cdk9.421E mice on a Dox diet for 72 h. Results are demonstrated by four biological replicates and three technical replicates. Statistical significance was calculated by two-tailed Student’s t test. Error bars correspond to mean ± SEM (*P < 0.05; **P < 0.01).