IndraLab

"For example, G9a methylates p53 and the myogenic regulator factor MyoD to inhibit their transactivation activity, whereas DNA ligase 1 methylated by G9a promotes the recruitment of UHRF1 and the maintenance of DNA methylation at DNA replication locus ( xref – xref )."

"For instance, G9a and GLP can methylate the tumor suppressor p53 [ xref ]."

"For example, there is convincing evidence that G9a and GLP physiologically methylate LIG1, p53, WIZ, Reptin, ACINUS, CDYL1 and other substrates (see xref ), with LIG1 being a particularly high-affinity substrate xref ."

"Accumulated evidence also indicates that PMTs play their physiological and pathogenic roles through methylating nonhistone substrates. xref , xref Some recent advancements in this aspect include the identification of SET7/9 substrates: the tumor suppressors p53 and pRb, E2F1, HIV transactivator Tat, estrogen receptor α (ERα), PCAF, DNMT1, AKA6, CENPC1, MeCP2, MINT, PPARBP, ZDH8, Cullin1, IRF1, TAF7/10 subunits of TATA box-binding protein complex and RelA subunit of NF-κB; xref – xref G9a substrates reptin, mAM, WIZ, CDYL1, CSB, C/EBP and the tumor suppressor p53;(Pless, 2008 #63; Rathert, 2008 #9; Huang, 2010 #308; Lee, 2010 #309) SUV39H1 substrate HP1α; xref SETDB1 substrate ING2; xref and SMYD3 substrate VEGF receptor 1. xref These PMT-involved nonhistone methylation events modulate the functions of diverse cellular targets, such as histone-remodeling apparatus, tumor suppressors, transcription regulators, and hormone receptors. xref , xref Some nonhistone targets, similar to histones, can be modified by multiple PMTs (e.g. site-specific methylations of the tumor suppressor p53 by SET7/9, SET8, G9a, GLP1, SMYD2 and PRMT5), xref , xref , xref , xref , xref which may resemble the histone-code scenario for epigenetic regulation."

"Moreover, as previously mentioned, G9a methylates the tumor suppressor p53, leading to its inactivation ( xref )."

"G9a and Glp specifically methylate p53 at Lys(373), resulting mainly in dimethylation."