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We conclude that Mdm4-S overexpression is a consequence of splicing defects in tumor cells rather than a cause of tumor evolution.
These results indicate that the rs4245739 polymorphism may contribute to a decreased cancer susceptibility and support the hypothesis that genetic variants in the MDM4 genes act as important modifiers of cancer risk.
our study is the first to identify miR (show MLXIP Proteins)-766 as a novel p53 (show TP53 Proteins) activator that functions by targeting MDM4 and thereby enhancing the p53 (show TP53 Proteins) signalling axis.
High MDM4 expression levels are associated with lymph node metastasis of gastric adenocarcinoma and influence the prognosis of patients with gastric adenocarcinoma
MDM4 rs4245739 A > C polymorphism appears to be associated with decreased cancer risk
analyses indicated that rs4245739 polymorphism in the MDM4 gene may play an important role in the etiology of cancer
analysis of linear and stapled peptides comprising 6-Me-tryptophan provides mechanistic insight into dual Mdm2 (show MDM2 Proteins)/Mdm4 antagonism and confirms L98 of Mdm4 as a mutable steric gate. The results also highlight a possible role of the flexible hinge region in determining Mdm2 (show MDM2 Proteins)/Mdm4 plasticity
we have herein demonstrated that ERalpha (show ESR1 Proteins) expression associates with MDM4 and MDM2 (show MDM2 Proteins) gene expression in primary breast invasive carcinoma samples
It is now clear that functional p53 (show TP53 Proteins) is critical to protect the genome from alterations that lead to tumorigenesis. The current understanding of the multiple ways p53 (show TP53 Proteins) contributes to genome stability and how two of its negative regulators, Mdm2 (show MDM2 Proteins) and Mdmx, induce genome instability will be described. [review]
results revealed an allosteric ligand-binding mechanism of the N-terminal domain of MdmX in which the ligand initially interacts with a compact core, followed by augmenting intermolecular interactions with intrinsic flexible regions
Data indicate that knockdown of the Mdm2 (show MDM2 Proteins) and Mdm4 caused dramatic accumulation of mutant p53 protein (show TP53 Proteins).
crystal structure of N-terminal domain of Mdmx bound to 15-residue p53 (show TP53 Proteins) peptide was determined; structure reveals that although principle features of Mdm2 (show MDM2 Proteins)-p53 (show TP53 Proteins) interaction are preserved, the Mdmx hydrophobic cleft on which the p53 (show TP53 Proteins) peptide binds is altered
The p53 (show TP53 Proteins)-null mice with the highest level of Mdm4 tended to have multiple tumours. Mdm4 transgenic mice in various genetic backgrounds shows synergy in tumour development in vivo. Mdm4 may thus serve as a therapeutic target in cancers.
These findings suggest that Mdm2 (show MDM2 Proteins) splice isoforms may play critical roles in the regulatory loop of p53 (show TP53 Proteins)/Mdm2 (show MDM2 Proteins)-Mdm4 via a RING domain-mediated biochemical mechanism.
both MDM2 (show MDM2 Proteins) and MDMX deletion-caused pancreatic defects are completely rescued by loss of p53 (show TP53 Proteins), verifying the crucial role of the MDM2 (show MDM2 Proteins) and/or MDMX in regulating p53 (show TP53 Proteins) in a spatio-temporal manner during the development, functional maintenance, and related disease progress of endocrine pancreas.
we failed to detect any increase in p53 (show TP53 Proteins) level in mutant oocytes, nor any other apoptotic marker, introgression of this targeted invalidation in p53 (show TP53 Proteins)-/- mice restored the fertility of females. This study is the first to show that Mdm2 (show MDM2 Proteins), but not Mdm4, has a critical role in oocyte survival and would be involved in premature ovarian insufficiency phenotype.
Data show that the Mdm4-p73 (show ARHGAP24 Proteins) axis cannot override the dominant role of p53 (show TP53 Proteins) in development and tumorigenesis and that Mdm4 and p73 (show ARHGAP24 Proteins) interaction during development and tumorigenesis suggests new insight into the role of p53 (show TP53 Proteins) family members.
MDM4/HIPK2 (show HIPK2 Proteins)/p53 (show TP53 Proteins) cytoplasmic assembly uncovers coordinated repression of molecules with anti-apoptotic activity during early DNA damage response.
MDMx degradation associated with neuronal death occurs via caspase (show CASP3 Proteins) activation in neurons, and that the progressive loss of MDMx protein represents a potential mechanism of Abeta (show APP Proteins)-induced neuronal death during disease progression in AD
our results show MDM4-MDM2 (show MDM2 Proteins)/p53 (show TP53 Proteins)-IGF1R (show IGF1R Proteins) as an original regulatory mechanism for CNS regeneration
Increased Mdm4-S mRNA levels might correlate with more aggressive cancers without encoding significant amounts of a potential oncoprotein.
results reveal a novel p53 (show TP53 Proteins)- and Mdm2 (show MDM2 Proteins)-independent oncogenic function of Mdmx that provides new insight into the many cancers that overexpress Mdmx.
This gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus, and shows structural similarity to p53-binding protein MDM2. Both proteins bind the p53 tumor suppressor protein and inhibit its activity, and have been shown to be overexpressed in a variety of human cancers. However, unlike MDM2 which degrades p53, this protein inhibits p53 by binding its transcriptional activation domain. This protein also interacts with MDM2 protein via the RING finger domain, and inhibits the latter's degradation. So this protein can reverse MDM2-targeted degradation of p53, while maintaining suppression of p53 transactivation and apoptotic functions. Alternatively spliced transcript variants encoding different isoforms have been noted for this gene.
double minute 4 protein
, mdm2-like p53-binding protein
, p53-binding protein Mdm4
, protein Mdm4
, MDM4-related protein 1
, double minute 4, human homolog of; p53-binding protein
, protein Mdmx
, Mdm4, transformed 3T3 cell double minute 4, p53 binding protein
, double minute 4 homolog
, transformed mouse 3T3 cell double minute 4