IndraLab

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KRAS methylates TP53. 6 / 6
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"Significantly, we demonstrated that disruption of the FA pathway compromised the oncogene K-ras G12D -induced arginine methylation of p53 mediated by the protein arginine methyltransferase 5 (PRMT5)."
27507053
sparser
"However, K-ras-induced arginine methylation of p53 was peaked at 2 hours and almost completely abated after 8-hour induction with 4-OHT inFanca −/− Lin − cells (Figure xref ), reminiscent of the short-lived oncogenic response described above."
27507053
sparser
"Mechanistic studies reveal that FA deficiency in HSPCs impairs oncogenic stress-induced G 1 cell-cycle checkpoint, resulting from a compromised K-ras G12D -induced arginine methylation of p53 mediated by the protein arginine methyltransferase 5 (PRMT5)."
27507053
sparser
"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."
27507053
sparser
"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 )."
27507053
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 )."
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