IndraLab
Statements
sparser
"SETD6 targets the RelA subunit of the transcription factor NF-κB to regulate inflammation ( xref ); SETD7 has many cancer-associated substrates, including p53, the DNA methyltransferase DNMT1, the phosphatase PPP1R12A, which regulates cell cycle through Rb, and many others ( xref ); SETD8 methylates histone H4 as well as p53 and proliferating cell nuclear antigen (PCNA) ( xref ; xref ; xref ); SETMAR is involved in repairing DNA damage and methylates the splicing factor snRNP70 ( xref ; xref )."
sparser
"Importantly, these phenotypes were shown to be a consequence of SET8 methylation of p53, and not an indirect effect of H4K20 methylation by SET8 since H4K20me1 levels were not changed in the experimental system upon manipulation of SET8 levels, and expression effects on specific target genes were abolished upon p53 knockdown [ xref ]."
reach
"Since then, a number of other KMTs, including SET9 (KMT5), SMYD2 (KMT3C), and SET 8 (KMT5A), which methylate p53 at specific C-terminal lysines, together with the lysine specific demethylase KDM1 (LSD1) which mediates p53 demethylation, have also been identified [XREF_BIBR] (XREF_FIG)."
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"XREF_BIBR, XREF_BIBR 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_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR which may resemble the histone-code scenario for epigenetic regulation."
reach
"Importantly, these phenotypes were shown to be a consequence of SET8 methylation of p53, and not an indirect effect of H4K20 methylation by SET8 since H4K20me1 levels were not changed in the experimental system upon manipulation of SET8 levels, and expression effects on specific target genes were abolished upon p53 knockdown [XREF_BIBR]."
sparser
"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."
reach
"SETD6 targets the RelA subunit of the transcription factor NF-kappaB to regulate inflammation; SETD7 has many cancer associated substrates, including p53, the DNA methyltransferase DNMT1, the phosphatase PPP1R12A, which regulates cell cycle through Rb, and many others; SETD8 methylates histone H4 as well as p53 and proliferating cell nuclear antigen (PCNA); SETMAR is involved in repairing DNA damage and methylates the splicing factor snRNP70."