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. 2016 Mar 4;7:10830. doi: 10.1038/ncomms10830

Figure 9. Proposed model of PTEN–SRF control of SMC differentiation.

Figure 9

(a) PTEN, SRF and myocardin form a higher order transcriptional complex facilitating interaction of SRF on SM gene promoters, but not IEG promoters (for example, cFos) thus maintaining the SMC contractile gene expression. (b) Stimuli that promote SMC dedifferentiation (for example, vascular injury/disease, PDGF) result in loss of PTEN and SRF interaction on SM gene promoters, nuclear exclusion of PTEN and a pool of SRF, and transcriptional repression of the SM differentiation program. Loss of PTEN promotes SRF–cofactor switching and enhanced SRF binding to IEG promoters.