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Epigenetics meets estrogen receptor: regulation of estrogen receptor by direct lysine methylation Zhou Q; Shaw PG; Davidson NEEndocr Relat Cancer 2009[Jun]; 16 (2): 319-23The nuclear hormone receptor estrogen receptor alpha (ERalpha) promotes cellular growth through ligand-dependent activation of specific target genes, a process which is targeted in the treatment of ERalpha-expressing breast cancers. ERalpha activity is regulated at the protein level by post-translational modifications including phosphorylation and acetylation. A study now shows that ERalpha can also be directly methylated at lysine 302 (K302) by SET7, a histone methyltransferase that is known to monomethylate H3K4 and is associated with transcriptional activation. It was shown that K302 methylation stabilizes ERalpha protein and is suggested to increase sensitivity of ERalpha to estrogens, enhancing transcription of estrogen response elements. Furthermore, SET7 methylation of K302 is enhanced by a breast cancer-associated mutation at K303 (K303R) in vitro. These findings provide an additional mechanism of SET7 mediated transcriptional activation, as well as potential insight into the complex regulation of ERalpha stability and ligand sensitivity.|*Methylation[MESH]|Epigenesis, Genetic/*physiology[MESH]|Estrogen Receptor alpha/*metabolism[MESH]|Histone Methyltransferases[MESH]|Histone-Lysine N-Methyltransferase/metabolism[MESH]|Humans[MESH]|Lysine/*metabolism[MESH] |
