Skip to main content

Advertisement

Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Fig. 4 | Cell & Bioscience

Fig. 4

From: KLF13 promotes porcine adipocyte differentiation through PPARγ activation

Fig. 4

Activation of porcine PPARγ transcription by KLF13. a The truncation analysis of PPARγ promoter. The truncated PPARγ promoter reporters (P1 ~ P4) were respectively co-transfected with pcDNA3.1-KLF13 or empty vector into PK15 cells. The dual-luciferase activity was measured 36 h after transfection. Values are represented as mean ± SD. (n = 3). b Schematics structure of KLF13 binding site mutation and deletion. c Effect of KLF13 binding site mutation and deletion on P1 promoter activity. Wild (P1), mutation type (P1 mut) and deletion type (P1 del) of PPARγ promoter reporter were respectively co-transfected with pcDNA3.1-KLF13 into PK15 cells. The dual-luciferase activity was measured 36 h after transfection. Values are represented as mean ± SD. (n = 3). d Effect of KLF13 binding site mutation and deletion on P2 promoter activity. Wild (P2), mutation type (P2 mut) and deletion type (P2 del) of PPARγ promoter reporter were respectively co-transfected with pcDNA3.1-KLF13 into PK15 cells. The dual-luciferase activity was measured 36 h after transfection. Values are represented as mean ± SD. (n = 3). e ChIP assay of KLF13 binding to porcine PPARγ promoter. The porcine ASVC were induced with adipogenic medium for 3 days, the cells were harvested for ChIP experiment. KLF13 binding region was detected by PCR. **P < 0.01

Back to article page