IndraLab
Statements
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"The current study demonstrated that the expression levels of EZH2 and P53 in tumor tissue and the proportion of cases with double positive expression significantly increased with increasing clinical stages of cancer, also confirming up-regulated expression of EZH2 and P53 with increasing stages."
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"Next, to investigate whether RITA induced senescence depends on p53 status, we treated the stable-p53-knockdown cell lines HN30-shp53 and HN31-shp53 with RITA and found that knockdown of p53 protein expression markedly reduced both the expression and phosphorylation of p53 (XREF_FIG)."
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"Thus we determined the need to isolate single cell DLD1 clones with p53-EGFP reporter expression that have fairly low basal EGFP expression and that could be induced to high EGFP expression upon exposure to small molecules that restore p53 pathway signaling in mutant p53 expressing DLD1 cells."
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"It is important to note that no prior study has linked p53 or p73 to the mechanism of action of either prodigiosin or its related structures and no prior study has demonstrated the ability of these compounds to restore p53 pathway signaling in mutant p53 expressing or p53-null cancer cells."
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"XREF_BIBR In addition to CDKN1A and p21 CIP1, other traditional p53 targets, such as GADD45 and 14-3-3sigma, also were up-regulated but perhaps not as a result of p53 activation given that 779e cells express no detectable p53 protein and that E47 repressed the expression of mutant p53 mRNA and protein in the other 4 lines (XREF_FIG A-F)."
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"The Chk signal transducers induce cell cycle arrest by phosphorylation of two critical effectors : inhibitory phosphorylation of the Cdc25 phosphatase results in CDK inactivation, while the activating phosphorylation of the p53 tumor suppressor stabilizes p53 and increases transcription of p53 target genes, including the cyclin dependent kinase inhibitor p21/CIP1/WAF-1."
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"1 For example, phosphorylation and acetylation of p53 have been shown to promote the expression of p53 transcriptional targets, whereas other modifications, such as ubiquitination, sumoylation, and neddylation have been associated with the suppression of p53 mediated transcription and p53 nuclear export."
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"This evidence may suggest that DNA hypomethylation of the p53 gene contributes to the enhanced p53 expression and causes abnormal apoptosis in lupus patients, a notion that needs further investigation.Several studies have demonstrated that methyl-CpG-binding domain 4 (MBD4) can be recruited by methylated DNA and thereby leading to the recruitment of histone modifying and chromatin-remodeling complexes to methylated sites [38,39]."
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"Although there was no significant difference in expression of CDKN1A, VDR, and TP53INP1 between CD24 + PC3 cells and CD24 - PC3 cells, the transfections of WT TP53, mutants TP53 R273H, TP53 V143A, and TP53 R280T, but not mutant TP53 R175H, induced the expression of these p53 target genes in CD24 - PC3 cells but not in CD24 + PC3 cells (XREF_FIG)."
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"Although there was no significant difference in expression of CDKN1A, VDR, and TP53INP1 between CD24 + PC3 cells and CD24 - PC3 cells, the transfections of WT TP53, mutants TP53 R273H, TP53 V143A, and TP53 R280T, but not mutant TP53 R175H, induced the expression of these p53 target genes in CD24 - PC3 cells but not in CD24 + PC3 cells (XREF_FIG)."
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"Although there was no significant difference in expression of CDKN1A, VDR, and TP53INP1 between CD24 + PC3 cells and CD24 - PC3 cells, the transfections of WT TP53, mutants TP53 R273H, TP53 V143A, and TP53 R280T, but not mutant TP53 R175H, induced the expression of these p53 target genes in CD24 - PC3 cells but not in CD24 + PC3 cells (XREF_FIG)."
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"Although there was no significant difference in expression of CDKN1A, VDR, and TP53INP1 between CD24 + PC3 cells and CD24 - PC3 cells, the transfections of WT TP53, mutants TP53 R273H, TP53 V143A, and TP53 R280T, but not mutant TP53 R175H, induced the expression of these p53 target genes in CD24 - PC3 cells but not in CD24 + PC3 cells (XREF_FIG)."
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"We generated female p53 (lox and lox)/FAK (+/+)/WapCre, p53 (lox and lox)/FAK (flox/+)/WapCre and p53 (lox and lox)/FAK (flox/-)/WapCre mice, and mice with WapCre mediated conditional expression of p53 (R270H), the mouse equivalent of human p53 (R273H) hot spot mutation, together with conditional deletion of FAK, P53 (R270H/+)/FAK (lox/+)/WapCre and p53 (R270H/+)/FAK (flox/-)/WapCre mice."