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In this review we focus on recent progress pertaining to the function and mechanism of RPs (show RPS3 ELISA Kits) in association with the MDM2-p53 (show TP53 ELISA Kits) tumor-suppression network, and the potential implications this surveillance network has for cancer development.
The study of 140 cases confirms that the incidence of MDM2/CDK4 (show CDK4 ELISA Kits) amplification is low (5%) in large and/or deep-seated (subfascial) lipomatous neoplasms with histological features of a lipoma (or lipoma variant).
Results suggest that inhibition the expression of c-mdm2 proto-oncogene (show RAB1A ELISA Kits) protein (MDM2) might be a potential target in non-small cell lung cancer (NSCLC) treatment.
analysis of linear and stapled peptides comprising 6-Me-tryptophan provides mechanistic insight into dual Mdm2/Mdm4 (show MDM4 ELISA Kits) antagonism and confirms L98 of Mdm4 (show MDM4 ELISA Kits) as a mutable steric gate. The results also highlight a possible role of the flexible hinge region in determining Mdm2/Mdm4 (show MDM4 ELISA Kits) plasticity
Study demonstrated in human breast cancer samples that MDM2 induces epithelial-to-mesenchymal transition by enhancing Snail (show SNAI1 ELISA Kits) expression in vitro and in vivo.
MDM2 and P53 (show TP53 ELISA Kits) polymorphisms combined contribute to both the risk and survival of prostate cancer.
Our data suggest that the expression of MDM2 confers sensitivity of cancer cells to IFNalpha/Nutlin-3a treatment. Moreover, our data also confirm positive effect of Nutlin even on p53 (show TP53 ELISA Kits)-deficient neoplasms.
Mdm2 overexpression and Cdc25C (show CDC25C ELISA Kits) downregulation delay cell cycle progression through the G2/M phase.
this study demonstrates that although early-onset breast cancer is thought to be associated with a strong genetic predisposition, this cannot be attributed to TP53 (show TP53 ELISA Kits) polymorphisms alone, or MDM2 SNP309:T>G in the population surveyed.
In this setting, it appears that mTORC1 activates senescence through HDM2 phosphorylation, facilitating a p53 (show TP53 ELISA Kits)-mediated response. Inhibition of mTORC1 by rapamycin decreases HDM2 phosphorylation and blocks activation of the senescence program in human cells.
genetic and biochemical data support a role for Mdm2 in cardiac growth control through the regulation of p53, the Pgc-1 family of transcriptional coactivators and the pivotal antioxidant Pink1
The availability of large-scale genomic profiling datasets, like those from The Cancer Genome Atlas Research Network, have provided the opportunity to evaluate the consequences of MDM2 amplification and SNP inheritance across high-quality tumor samples from diverse cancer indications. [review]
findings document contrasting effects of ATM (show ATM ELISA Kits)-Mdm2 signaling on p53 (show TP53 ELISA Kits) tumor suppression and reveal that destabilizing Mdm2 by promoting its phosphorylation by ATM (show ATM ELISA Kits) would be effective in treating oncogene (show RAB1A ELISA Kits)-induced malignancies.
the existence of an unusual functional interplay between STATs and CREB (show CREB1 ELISA Kits) at the onset of adipogenesis through shared CRTC cofactors, is reported.
Mdm2 expression is required for cell survival even in the absence of p53 (show TP53 ELISA Kits). Moreover, results suggest that p73 (show ARHGAP24 ELISA Kits) compensates for loss of p53 (show TP53 ELISA Kits).
In Fmr1 (show FMR1 ELISA Kits) KO neurons, Mdm2 is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 (show MEF2C ELISA Kits) activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (show TSFM ELISA Kits) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (show FMR1 ELISA Kits) KO. Expression of a dephosphomimetic of Mdm2 rescues PSD-95 (show DLG4 ELISA Kits) ubiquitination, degradation and synapse elimination in Fmr1 (show FMR1 ELISA Kits) KO neurons.
MDM2 is a non-redundant survival factor for proximal tubular cells by protecting them from spontaneous p53 (show TP53 ELISA Kits) overexpression-related cell death.
The case emphasizes that MDM2 expression represents a possible pitfall in the diagnosis of spindle cell tumors. The differential diagnostic distinction between FDCS and a dedifferentiated liposarcoma is discussed.
MDM2 is involved in fibroblast activation, mediating renal tubulointerstitial fibrosis via a p53 (show TP53 ELISA Kits)-independent pathway dependant on Notch1 (show NOTCH1 ELISA Kits) ubiquitination and proteasome degradation.
These findings suggest that Mdm2 splice isoforms may play critical roles in the regulatory loop of p53 (show TP53 ELISA Kits)/Mdm2-Mdm4 (show MDM4 ELISA Kits) via a RING domain-mediated biochemical mechanism.
This gene is a target gene of the transcription factor tumor protein p53. The encoded protein is a nuclear phosphoprotein that binds and inhibits transactivation by tumor protein p53, as part of an autoregulatory negative feedback loop. Overexpression of this gene can result in excessive inactivation of tumor protein p53, diminishing its tumor suppressor function. This protein has E3 ubiquitin ligase activity, which targets tumor protein p53 for proteasomal degradation. This protein also affects the cell cycle, apoptosis, and tumorigenesis through interactions with other proteins, including retinoblastoma 1 and ribosomal protein L5. More than 40 different alternatively spliced transcript variants have been isolated from both tumor and normal tissues.
E3 ubiquitin-protein ligase Mdm2
, Mdm2, p53 E3 ubiquitin protein ligase homolog
, Mdm2, transformed 3T3 cell double minute 2, p53 binding protein
, double minute 2, human homolog of; p53-binding protein
, oncoprotein Mdm2
, double minute 2 protein
, p53-binding protein Mdm2