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. 2015 Aug 31;2(8):700–702. doi: 10.18632/oncoscience.222

Figure 1. Model of p53 methylation function in tumorigenesis.

Figure 1

A. p53-dependent transcription of pro-apoptotic genes is activated in response to oncogenic cyclin D1T286A/CDK4. B. In the presence of high level of PRMT5, cyclin D1T286A/CDK4 phosphorylaties MEP50, which in turn catalytically actives PRMT5 on p53 with the consequence of transcriptional inactivation, eventually leading to malignant transformation.