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. 2015 Sep 30;6:8419. doi: 10.1038/ncomms9419

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KLF4 protein is coordinately regulated by PRMT5-dependent arginine methylation and VHL-dependent ubiquitylation. Following genotoxic stress, disruption of PRMT5-mediated KLF4 methylation leads to abrogation of KLF4 accumulation, which, in turn, attenuates cell cycle arrest. During the tumorigenesis, downregulation of Bax or upregulation of several oncogenes due to aberrant KLF4 accumulation results in mammary tumor initiation and progression.