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. 2009 May 6;284(27):18184–18193. doi: 10.1074/jbc.M109.007096

FIGURE 6.

FIGURE 6.

A model for how KLF5 reverses function in transcriptional regulation of p15 in the context of TGFβ. Without TGFβ, some KLF5 associates with Miz-1, Myc, and possibly other molecules on the Inr DNA elements to block p15 transcription, whereas other KLF5 associates with Smad4 in the nucleus. When TGFβ signaling is activated, Smad2 and Smad3 are phosphorylated and translocated into the nucleus (32), where they recruit p300 to the KLF5-Smad4 complex to acetylate KLF5 at lysine 369. Acetylated KLF5-Smad complex then binds to the SBE, assembling with p15 factors such FOXO3 and Miz-1 and altering the existing KLF5 transcriptional assembly bound to the SPS2 and Inr elements to release the transcription of p15. Question marks indicate unknown molecules.