"Remarkably, a homozygous Mdm2 C305F background reversed the accumulation of p53."
"The Mdm2 C305F mutation, which disrupts the binding of ribosomal proteins L11 and L5 to Mdm2 XREF_BIBR, causes an attenuation of p53 signaling, suggesting that the Mdm2 C305F mutation may alter the progression, rather than initiation, of prostate tumorigenesis in a similar way as p53 heterozygosity."
"Furthermore, the MDM2 C305F, which is defective in RPL11- and RPL5- binding in vitro and in vivo, has been shown to impair the p53 response to ribosomal stress in animals, strongly demonstrating the essential role of RP-MDM2 interactions in activation of p53 upon ribosomal stress."
"Upon induction of the Rps19 deficiency, Mdm2 C305F reversed the p53 response and improved expansion of hematopoietic progenitors in vitro, and ameliorated the anemia in vivo."
"MDM2 C305F mutation attenuates p53 activation in colon tumors."
"Further evidence supporting the adverse effect of high p53 activity in promoting obesity was demonstrated in mutant MDM2 C305F mice that have impaired p53 regulation of lipid metabolism."
"23 As a working model, we hypothesized that if the p53 response in Rps19 deficient mice is mediated through the 5S RNP-Mdm2 interaction, the Mdm2 C305F background should reverse the p53 activity and subsequently improve the erythroid phenotype of these mice."
"Reduction of the p53 activity in Rps19 deficient hematopoietic stem and progenitor cells by Mdm2 C305F normalized their viability and improved their proliferative capacity, resulting in significantly increased expansion of these cells in vitro."
"Mdm2 C305F mutation attenuates p53 response to ribosome biogenesis stress."