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. 1997 Aug 1;11(15):1987–1998. doi: 10.1101/gad.11.15.1987

Figure 3.

Figure 3

 Transcription factor activity of PPARγ is required for its negative regulatory function on cell growth. (Left) Schematic representations of wild-type PPARγ1, PPARγ2, or mutant PPARγ2 cDNAs. NIH–M1 cells contain PPARγ expression vector, which lacks the first 127 amino acids located in the amino terminus. NIH–M2 cells express a PPARγ2 receptor in which cystein residues at the DNA-binding domain at positions 156 and 159 have been changed to serine. NIH–CD cells express a truncated form of PPARγ2, which lacks the conserved carboxyl-terminal transactivation domain. (Right) Effects of pioglitazone treatment on the growth rate of cells expressing wild-type or mutant forms of PPARγ. Cell numbers were determined after 5 days treatment without or with 5 μm pioglitazone. Decrease in the cell number in treated plates was represented as relative change to untreated control plates. The data represent the average of at least three independent experiments.