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Human MDM2 Protein expressed in Wheat germ - ABIN1310600
Zhang, Zhong, Chen: LC-MS/MS-based targeted proteomics quantitatively detects the interaction between p53 and MDM2 in breast cancer. in Journal of proteomics 2016
Results suggest that inhibition the expression of c-mdm2 proto-oncogene (show RAB1A Proteins) 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 Proteins) antagonism and confirms L98 of Mdm4 (show MDM4 Proteins) as a mutable steric gate. The results also highlight a possible role of the flexible hinge region in determining Mdm2/Mdm4 (show MDM4 Proteins) plasticity
Study demonstrated in human breast cancer samples that MDM2 induces epithelial-to-mesenchymal transition by enhancing Snail (show SNAI1 Proteins) expression in vitro and in vivo.
MDM2 and P53 (show TP53 Proteins) 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 Proteins)-deficient neoplasms.
Mdm2 overexpression and Cdc25C (show CDC25C Proteins) 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 Proteins) 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 Proteins)-mediated response. Inhibition of mTORC1 by rapamycin decreases HDM2 phosphorylation and blocks activation of the senescence program in human cells.
Data find the MDM2 SNP del1518 del variant to be associated with reduced risk of endometrial cancer among individuals carrying the SNP309TT genotype nut no association with ovarian cancer risk.
Data suggest that Per2 (show PER2 Proteins) is not only a tumor suppressor gene but can also be regarded as a regulator of MDM2-TP53 (show TP53 Proteins) pathway.
results suggest overexpression of MDM2 is closely linked to inhibition of p53 (show TP53 Proteins)-dependent apoptosis of Theileria parva (show PARVA Proteins)-infected lymphocytes; aberrant expression of host lymphocyte MDM2 induced by cytoplasmic existence of T. parva (show PARVA Proteins), directly and/or indirectly, is associated with aspects of this type of transformation of T. parva (show PARVA Proteins)-infected lymphocytes
mutant Mdm2 was unable to rescue a p53 (show TP53 Proteins)-induced apoptotic phenotype.
Data indicate that knockdown of the Mdm2 and Mdm4 (show MDM4 Proteins) caused dramatic accumulation of mutant p53 protein (show TP53 Proteins).
Together with p53 (show TP53 Proteins), provides an experimental model for characterizing drugs and genes that affect p53 (show TP53 Proteins) signaling.
Data show that liver-specific expression of p53 (show TP53 Proteins)-negative regulator mdm2 leads to growth retardation and fragile liver in zebrafish.
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 Proteins)-Mdm2 signaling on p53 (show TP53 Proteins) tumor suppression and reveal that destabilizing Mdm2 by promoting its phosphorylation by ATM (show ATM Proteins) would be effective in treating oncogene (show RAB1A Proteins)-induced malignancies.
the existence of an unusual functional interplay between STATs and CREB (show CREB1 Proteins) 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 Proteins). Moreover, results suggest that p73 (show ARHGAP24 Proteins) compensates for loss of p53 (show TP53 Proteins).
In Fmr1 (show FMR1 Proteins) KO neurons, Mdm2 is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 (show MEF2C Proteins) activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (show TSFM Proteins) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (show FMR1 Proteins) KO. Expression of a dephosphomimetic of Mdm2 rescues PSD-95 (show DLG4 Proteins) ubiquitination, degradation and synapse elimination in Fmr1 (show FMR1 Proteins) KO neurons.
MDM2 is a non-redundant survival factor for proximal tubular cells by protecting them from spontaneous p53 (show TP53 Proteins) 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 Proteins)-independent pathway dependant on Notch1 (show NOTCH1 Proteins) ubiquitination and proteasome degradation.
These findings suggest that Mdm2 splice isoforms may play critical roles in the regulatory loop of p53 (show TP53 Proteins)/Mdm2-Mdm4 (show MDM4 Proteins) via a RING domain-mediated biochemical mechanism.
both MDM2 and MDMX (show MDM4 Proteins) deletion-caused pancreatic defects are completely rescued by loss of p53 (show TP53 Proteins), verifying the crucial role of the MDM2 and/or MDMX (show MDM4 Proteins) in regulating p53 (show TP53 Proteins) in a spatio-temporal manner during the development, functional maintenance, and related disease progress of endocrine pancreas.
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
, Mdm2 p53 binding protein homolog
, double minute 2 protein
, p53-binding protein Mdm2
, MDM2 alpha
, double minute 2 homolog
, double minute 2
, MDM2-like protein
, transformed mouse 3T3 cell double minute 2
, murine double minute 2 homolog