IndraLab
Statements
TP53 is modified
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"In that category, the most sensitive and specific biomarker (more properly, “biosignature”) for detecting ovarian cancer currently appears to be a panel of six serum proteins (leptin, prolactin, osteopontin, insulin-like growth factor II, macrophage inhibitory factor and CA125), which has been reported to identify ovarian cancer as early as stage I with a striking 99.3% positive predictive value and 99.2% negative predictive value. xref The second biomarker category aims to predict outcome; examples include p53, p21, Ki-67, and HOXA11 DNA methylation. xref – xref The third category is similar to the second but specifically aims to predict which patients will respond to a particular treatment, as is the case for the biomarker upon which this review is focused."
sparser
"It would also be of interest to examine how cytosine methylation at the 5′-C of the CpG sites at Fapy•dG 248 and 273 may influence replicative bypass of Fapy•dG, as we have shown previously that in p53 codon 273 cytosine methylation increases MF of a bulky dG adduct significantly [ xref ]."
sparser
"In order to improve our understanding of the Smyd2 catalytic cycle, here we carried out μ‐second MD simulations of the following systems (see Fig. xref ): Smyd2 in complex with AdoMet cofactor (Model‐A); Smyd2‐AdoMet‐p53 peptide (unmethylated) complex (Model‐B); Smyd2‐AdoHcy‐p53 peptide (methylated at Lys370) complex (Model‐C); and Smyd2‐AdoMet in complex with the p53 peptide methylated at Lys372 (Model‐D)."
sparser
"These results disfavour a role for JMJD3 in the regulation of p53 C-terminal methylation, however, we cannot rule out that JMJD3 is involved in regulating p53 methylation at other lysine residues than the tested ones, or that additional co-factors are required for an efficient enzymatic removal of methylation."
sparser
"In general, while methylation of p53 at K370, K373 and K382 represses p53 transcriptional activities, methylation at K372 enhances p53 activities. xref – xref Since KDM3A knockdown activated the expression of p53-dependent genes, we reasoned that increasing p53 methylation enhanced its transcriptional activities."
sparser
"Lysine (K) and arginine (R) residues in p53 can be methylated, and a growing number of studies in recent years have shown that p53 methylation takes place during the DNA damage response. xref – xref Methylation of lysine and arginine residues in histones has long been known to impact chromatin structure and gene expression. xref In recent years, the methylation of p53 has emerged as an important modification that affects its function in various processes, such as cell cycle arrest, DNA repair, senescence, apoptosis, and tumourigenesis. xref Whether p53 is activated or depressed depends on the location of the modification and the number of methyl groups attached. xref Protein arginine N -methyl transferase 5 (PRMT5) was first shown to methylate p53 at several arginine residues (R333, R335, and R337) in the tetramerization domain, xref which specifically controls the functions of p53 in cell cycle arrest and is suggested to inactivate p53 during lymphomagenesis. xref , xref There are three different lysine methyl transferases (KMTs) that could mono-methylate p53, and there are at least two KMTs could di-methylate p53. xref "
sparser
"C-terminal lysine residues of p53 are methylated in vivo at K370, K372, K373, and K382 by histone lysine methyl transferases, Smyd2, SET9, G9a/Glp, and Set8, respectively. xref – xref While K372 methylation by SET9 in human cells enhanced p53 transcriptional activities, the role of p53 methylation in the mouse by Set7/9 was controversial. xref – xref However, it should be pointed out that the results from mouse embryonic fibroblasts in the mouse study might be inappropriate to apply to human epithelial cells."
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"QPCR analysis also showed that Mll2 Gdf9 cKO oocytes overexpressed several apoptosis associated genes (XREF_TABLE), including p53 (transformation related protein 53; TRP53) and Setd7 (SET domain lysine methyltransferase 7, also know as Set7/9) (XREF_TABLE and XREF_SUPPLEMENTARY), which methylates p53 and prevents its degradation XREF_BIBR."
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"Originally defined as a critical layer of p53 regulation in human cell lines, p53 lysine methylation by Set7/9 (also called Setd7) was proposed to fulfill a similar function invivo in the mouse, promoting p53 acetylation, stabilization, and activation upon DNA damage (Kurash etal., 2008)."
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."
sparser
"For example, H4R3 can be methylated by PRMT1, PRMT5, PRMT6, and PRMT7; xref – xref TP53 can be methylated by PRMT3 and PRMT5; xref , xref and H3R2 can be methylated by PRMT5, PRMT6, and PRMT7. xref , xref To further understand the roles of each PRMT in cell biology, highly selective and cell-active inhibitors of each PRMT are needed."
reach
"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."
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"In conclusion, the present study, using an innovative in vivo model integrating the stress responsive Gadd45beta-luciferase transgene and inducible oncogenes (LSL-K-ras G12D and Myc ER), uncovers two novel and significant findings : (i) normal HSPCs utilize arginine methylation of p53 by PRMT5 to orchestrate long lasting oncogenic response."
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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."
sparser
"C-terminal lysine residues of p53 are methylated in vivo at K370, K372, K373, and K382 by histone lysine methyl transferases, Smyd2, SET9, G9a/Glp, and Set8, respectively. xref – xref While K372 methylation by SET9 in human cells enhanced p53 transcriptional activities, the role of p53 methylation in the mouse by Set7/9 was controversial. xref – xref However, it should be pointed out that the results from mouse embryonic fibroblasts in the mouse study might be inappropriate to apply to human epithelial cells."
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 ]."
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"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)."
sparser
"As a methyltransferase, SET8 methylates lysine 382 of p53 to modulates p53 activity so as to change its transcriptional activity for downstream targets, furthermore, SET8 knockdown has been shown to upregulate cells’ sensitivity to cell death and cell cycle arrest following DNA damage by suppressing the biological function of p53 xref ."
sparser
"C-terminal lysine residues of p53 are methylated in vivo at K370, K372, K373, and K382 by histone lysine methyl transferases, Smyd2, SET9, G9a/Glp, and Set8, respectively. xref – xref While K372 methylation by SET9 in human cells enhanced p53 transcriptional activities, the role of p53 methylation in the mouse by Set7/9 was controversial. xref – xref However, it should be pointed out that the results from mouse embryonic fibroblasts in the mouse study might be inappropriate to apply to human epithelial cells."
reach
"Next, we determined whether PIMT methylates p53 under physiological conditions through nano-LC-ESI-MS/MS analysis of endogenous p53 purified from U2OS cells or ectopic expressed p53 purified from H1299 cells under conditions in which the PIMT catalyzed methylation of the isoaspartyl residues was stable enough for detection (XREF_FIG)."
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"XREF_BIBR, XREF_BIBR - XREF_BIBR The di methylation of p53 K373 by G9a and GLP (also known as KMT1D or EHMT1), a closely related methyltransferase that shares 80% sequence identity with G9a in their respective SET domains and forms a heterodimer with G9a, results in the inactivation of p53, whose loss of function is implicated in over 50% of cancers."
reach
"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."
sparser
"Oncogenic growth of such tumours is associated with reduced p53 activity caused by overexpression of one or more epigenetic regulators that post-translationally modify p53 protein and impair its tumour-suppressor functions, including Aurora A kinase that phosphorylates p53 (S212/S312) and methyltransferases that methylate p53 such as Smyd2 (K370), Glp/G9a (K373) and PR-Set7 (K382)."
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"Because transcription factor occupancy can affect DNA methylation levels and DMR1 is within a p53 binding site at the DINO/CDKN1A locus, we examined whether TP53 status is associated with a differential methylation of p53 bound sites elsewhere in the genome (Younger et al., 2015)."
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"QPCR analysis also showed that Mll2 Gdf9 cKO oocytes overexpressed several apoptosis associated genes (XREF_TABLE), including p53 (transformation related protein 53; TRP53) and Setd7 (SET domain lysine methyltransferase 7, also know as Set7/9) (XREF_TABLE and XREF_SUPPLEMENTARY), which methylates p53 and prevents its degradation XREF_BIBR."
reach
"QPCR analysis also showed that Mll2 Gdf9 cKO oocytes overexpressed several apoptosis associated genes (XREF_TABLE), including p53 (transformation related protein 53; TRP53) and Setd7 (SET domain lysine methyltransferase 7, also know as Set7/9) (XREF_TABLE and XREF_SUPPLEMENTARY), which methylates p53 and prevents its degradation 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."
sparser
"In the present study, we have determined the TP53 CpG methylation profile in the substituted segment of Hupki embryonic fibroblasts and compared it to the methylation profile of the same segment when present in normal human neonatal fibroblasts, using two independent assays, including the combined bisulfite-restriction analysis (COBRA) [ xref ], and sodium bisulfite genomic sequencing [ xref ]."
sparser
"These data confirm that site‐specific changes of intragenic TP53 CpG methylation are extrinsically inducible, and suggest that human cancer progression is mediated in part by dysregulation of damage‐inducible intragenic CpG demethylation that alters TP53 P1/P2 isoform expression. © 2015 The Authors."
sparser
"For example, H4R3 can be methylated by PRMT1, PRMT5, PRMT6, and PRMT7; xref – xref TP53 can be methylated by PRMT3 and PRMT5; xref , xref and H3R2 can be methylated by PRMT5, PRMT6, and PRMT7. xref , xref To further understand the roles of each PRMT in cell biology, highly selective and cell-active inhibitors of each PRMT are needed."
Methyltransferase activity affects TP53
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Methyltransferase activity methylates TP53. 4 / 4
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Methyltransferase activity methylates TP53 on K372. 3 / 3
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"It has recently been shown that p53 can be methylated at K372 by Set9 methyltransferase,[ xref ] and that the PHD finger of ING1/2 is required for p53 activity.[ xref , xref , xref ] Addition of the p53K372me3 or p53K372me1 peptides resulted in small chemical shift changes in the ING2 (and homologous ING1) PHD finger, however the binding was at least tenfold weaker than the interaction with unmodified H3."
Methyltransferase activity methylates TP53 on R379. 1 / 1
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Transferase affects TP53
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Transferase methylates TP53 on lysine. 2 / 2
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"C-terminal lysine residues of p53 are methylated in vivo at K370, K372, K373, and K382 by histone lysine methyl transferases, Smyd2, SET9, G9a/Glp, and Set8, respectively. xref – xref While K372 methylation by SET9 in human cells enhanced p53 transcriptional activities, the role of p53 methylation in the mouse by Set7/9 was controversial. xref – xref However, it should be pointed out that the results from mouse embryonic fibroblasts in the mouse study might be inappropriate to apply to human epithelial cells."
Transferase methylates TP53 on K382. 2 / 2
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Transferase methylates TP53 on arginine. 1 / 1
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Transferase methylates TP53 on K373. 1 / 1
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"There are several findings that highlight the significance of our study: 1) FA HSPCs displayed an aberrant short-lived response to oncogenic stress induced by activated K-ras or c-Myc; 2) Fanca deficiency compromises K-ras G12D -induced arginine methylation of p53 accompanied by downregulated PRMT5; 3) forced expression of PRMT5 inFanca −/− HSPCs prolonged oncogenic response and delayed leukemia development in irradiated recipient mice."
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"Remarkably, we showed that Fanca deficiency compromised K-ras G12D -induced arginine methylation of p53 accompanied by downregulated PRMT5 and that forced expression of PRMT5 inFanca −/− HSPCs prolonged oncogenic response and delayed leukemia development in irradiated recipient mice (Figure xref )."
sparser
"Downregulation of Protein Arginine Methyltransferase 5 (PRMT5) led to compromised K-ras G12D -induced arginine methylation of p53 in FANCA deficient cells, thereby demonstrating an arginine methylation-dependent FA-p53 interaction, as forced expression of PRMT5 inFANCA −/− HSPCs prolonged oncogenic response and delayed leukemia development in irradiated recipient mice ( xref )."
Selenium atom affects TP53
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Selenium atom leads to the methylation of TP53. 4 / 4
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"Taken together, long-term Se consumption not only affects selenoprotein enzyme activities, homocysteine, tissue Se concentrations, and global genomic DNA methylation but also increases exon specific DNA methylation of the p53 gene in a Se-dose-dependent manner in rat liver and colon mucosa."
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"The study whether selenium affects the methylation of the p53 gene was investigated, and it was found that supranutritional dose of selenium significantly increased the exon specific DNA methylation of the p53 gene (in exons 5-8) in liver and colon mucosa of rats compared with this in animals fed with the selenium deficient diet [XREF_BIBR]."
Arsenic atom affects TP53
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PKMT affects TP53
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"Similarly, bisulfite sequencing analysis confirmed in HDFs that UVA irradiation caused demethylation of CpG in the p53 promoter region, while DNMT1 up-regulation could methylate CpG islands of p53, although the demethylation caused by UVA and DNMT1 induced methylation did not occurred at the same CpG islands (XREF_FIG)."
Folic acid affects TP53
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Folic acid leads to the methylation of TP53. 2 / 2
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Folic acid leads to the methylation of TP53. 1 / 1
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"At 14 weeks of age, both maternal and postweaning folic acid supplementation significantly increased DNA methylation of the Ppar-gamma, p53, and p16 genes (p < 0.05) whereas only postweaning FA supplementation significantly increased DNA methylation of the ER-alpha and Apc genes (p < 0.05)."
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"Additionally, in C57BL/6 mice, maternal and post-weaning folate-deficient (0.4 mg/kg diet) diets were shown to modulate colorectal cancer development by inducing p53 promoter hypomethylation in adults and adenomatous polyposis coli (APC) promoter hypermethylation in APC offspring, respectively [55]."
sparser
"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 ] ( xref )."
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"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)."
Particulate Matter affects TP53
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Particulate Matter methylates TP53. 3 / 3
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Transferases, G9a and Glp affects TP53
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Transferases, G9a and Glp methylates TP53 on K373. 2 / 2
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Selenomethionine affects TP53
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Glyphosate affects TP53
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Glyphosate leads to the methylation of TP53. 2 / 2
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"For example, the 53BP1 tandem-Tudor domain binds to H4K20me3 and dimethylated p53 [XREF_BIBR, XREF_BIBR], and that of PHF20 has been shown to bind to lysine dimethylation of histones [XREF_BIBR] and p53 [XREF_BIBR]; in the latter case, PHF20 binding to p53 stabilizes p53 and promotes its activation during DNA damage response [XREF_BIBR]."
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"To further define the specificity, we examined interactions of the 53BP1 tandem Tudor domain with the other two methylated species of p53, known p53K370me2 XREF_BIBR, and yet to be identified p53K372me2, using NMR and fluorescence spectroscopy, and determined the 1.5 A and 1.9 A resolution crystal structures of the complexes (XREF_FIG)."
Set9 histone-lysine N-methyltransferase affects TP53
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SCF Fbxo22 affects TP53
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Methyltransferases affects TP53
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Methyltransferases methylates TP53. 1 / 1
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"Oncogenic growth of such tumours is associated with reduced p53 activity caused by overexpression of one or more epigenetic regulators that post-translationally modify p53 protein and impair its tumour-suppressor functions, including Aurora A kinase that phosphorylates p53 (S212/S312) and methyltransferases that methylate p53 such as Smyd2 (K370), Glp/G9a (K373) and PR-Set7 (K382)."
Methyltransferases methylates TP53 on K372. 1 / 1
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JMJD3 demethylase affects TP53
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"GLP1 methylates its canonical substrate histone H3 as well as diverse biologically relevant non-histone substrates such as DNMT3A (Chang et al., 2011), p53 (Huang et al., 2010), C/EBP-β (Pless et al., 2008), Reptin (Lee et al., 2010), and MyoD (Ling et al., 2012) without consensus substrate-recognizing sequences."
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."
G9a and GLP affects TP53
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Air Pollutants affects TP53
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Valproic acid affects TP53
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Sodium arsenite affects TP53
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Resveratrol affects TP53
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Resveratrol leads to the methylation of TP53. 1 / 1
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P53K373me2 affects TP53
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P16 ink4a promoter affects TP53
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Daphnetin affects TP53
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Bisphenol A affects TP53
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Aflatoxin B1 affects TP53
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VHL30 affects TP53
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UVA affects TP53
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Tudor domain affects TP53
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Tudor domain methylates TP53. 1 / 1
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"To further define the specificity, we examined interactions of the 53BP1 tandem Tudor domain with the other two methylated species of p53, known p53K370me2 XREF_BIBR, and yet to be identified p53K372me2, using NMR and fluorescence spectroscopy, and determined the 1.5 A and 1.9 A resolution crystal structures of the complexes (XREF_FIG)."
Set domain affects TP53
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Set domain methylates TP53 on K372. 1 / 1
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"Although the mechanism linking these methyltransferases and CK is unknown, it noteworthy that SMYD2 may act as an oncogene by promoting the methylation of p53 and of the retinoblastoma tumor suppressor protein (RB) [56–57], and that SMYD3 promotes MAP3K2 methylation, inducing genomic instability by activation of Ras/Aurora kinase A-driven mechanisms [55, 58–59]."
SET1C affects TP53
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"We identify that P53 contains a sequence similar to the N-terminal loop of MLL2 SET , and demonstrate that K305 of P53 could be methylated by KMT2 family complexes except for SET1A. Our results provide an important implication of functional interplay between P53 and KMT2 family complexes, and also suggest the possible broad landscape of non-histone substrate for KMT2 family methyltransferases."
SCF FBXO22 affects TP53
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SCF FBXL17 affects TP53
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PRMTs affects TP53
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PRMT5Delta affects TP53
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PM2.5 affects TP53
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PKMTs affects TP53
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OLE affects TP53
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KMTase affects TP53
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KMT2 affects TP53
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KMT2 family affects TP53
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JMJD3-demethylase affects TP53
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Isocitrates affects TP53
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Isocitrates leads to the methylation of TP53. 1 / 1
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"Secondary GBM derives from lower-grade gliomas, affects the younger population, has a more favourable prognosis and is commonly related to loss of chromosome 19q, O -methylguanine-DNA-methyltransferase (MGMT) promoter methylation (on chromosome 10q26), TP53 and isocitrate dehydrogenase 1 (IDH1) mutations [23,24]."
HMTs affects TP53
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H4 affects TP53
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DNMTs affects TP53
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DNMT3beta affects TP53
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DNA methyltransferase inhibitor affects TP53
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D1T286A affects TP53
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BAY598 affects TP53
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AuNP affects TP53
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"AuNP exposure had dose specific changes in promoter methylation of Gsr (CpG # 4 and CpG # 6, p = 0.018 and p = 0.012, respectively), Pparg (CpG # 3, p = 0.031) and tumor protein P53 (trp53) (CpG # 1, p = 0.028) with low and high dose, 60 and 250 nm, respectively (i.e., dose effect) (XREF_FIG, XREF_TABLE)."
ARF affects TP53
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5-methylcytosine affects TP53
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5-methylcytosine methylates TP53. 1 / 1
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2-amino-3-phosphonopropanoic acid leads to the methylation of TP53. 1 / 1
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(20S)-ginsenoside Rg3 affects TP53
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(20S)-ginsenoside Rg3 leads to the methylation of TP53. 1 / 1
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2'-deoxyzebularine 5'-phosphate affects TP53
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2'-deoxyzebularine 5'-phosphate leads to the methylation of TP53. 1 / 1
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