Use your antibodies-online credentials, if available.
Select your species
Mdm2 overexpression and Cdc25C (显示 CDC25C ELISA试剂盒) 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 (显示 TP53 ELISA试剂盒) 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 (显示 TP53 ELISA试剂盒)-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 (显示 PER2 ELISA试剂盒) is not only a tumor suppressor gene but can also be regarded as a regulator of MDM2-TP53 (显示 TP53 ELISA试剂盒) pathway.
Simulation of HEY1 (显示 HEY1 ELISA试剂盒) Ser (显示 SIGLEC1 ELISA试剂盒)-68 phosphorylation prevents its interaction with p53 (显示 TP53 ELISA试剂盒), RPL11 (显示 RPL11 ELISA试剂盒) and MDM2 and abolishes HEY1 (显示 HEY1 ELISA试剂盒) migration to nucleolar caps (显示 CAPS ELISA试剂盒) upon ribosomal stress. Our findings uncover a novel mechanism for cross-talk between Notch (显示 NOTCH1 ELISA试剂盒) signalling and nucleolar stress
we have herein demonstrated that ERalpha (显示 ESR1 ELISA试剂盒) expression associates with MDM4 (显示 MDM4 ELISA试剂盒) and MDM2 gene expression in primary breast invasive carcinoma samples
overview of apoptosis and cell-cycle arrest in human cancer, highlighting the frequent occurrence of MDM2 amplification in sarcoma and the role of SNP309 and SNP285 in regulating MDM2 expression and cancer risk [review]
quantitative detection of p53 (显示 TP53 ELISA试剂盒)-MDM2 interaction in breast cells and tissue samples.
It is now clear that functional p53 (显示 TP53 ELISA试剂盒) is critical to protect the genome from alterations that lead to tumorigenesis. The current understanding of the multiple ways p53 (显示 TP53 ELISA试剂盒) contributes to genome stability and how two of its negative regulators, Mdm2 and Mdmx (显示 MDM4 ELISA试剂盒), induce genome instability will be described. [review]
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 (显示 ATM ELISA试剂盒)-Mdm2 signaling on p53 (显示 TP53 ELISA试剂盒) tumor suppression and reveal that destabilizing Mdm2 by promoting its phosphorylation by ATM (显示 ATM ELISA试剂盒) would be effective in treating oncogene (显示 RAB1A ELISA试剂盒)-induced malignancies.
the existence of an unusual functional interplay between STATs and CREB (显示 CREB1 ELISA试剂盒) at the onset of adipogenesis through shared CRTC cofactors, is reported.
Mdm2 expression is required for cell survival even in the absence of p53 (显示 TP53 ELISA试剂盒). Moreover, results suggest that p73 (显示 ARHGAP24 ELISA试剂盒) compensates for loss of p53 (显示 TP53 ELISA试剂盒).
In Fmr1 (显示 FMR1 ELISA试剂盒) KO neurons, Mdm2 is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 (显示 MEF2C ELISA试剂盒) activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (显示 TSFM ELISA试剂盒) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (显示 FMR1 ELISA试剂盒) KO. Expression of a dephosphomimetic of Mdm2 rescues PSD-95 (显示 DLG4 ELISA试剂盒) ubiquitination, degradation and synapse elimination in Fmr1 (显示 FMR1 ELISA试剂盒) KO neurons.
MDM2 is a non-redundant survival factor for proximal tubular cells by protecting them from spontaneous p53 (显示 TP53 ELISA试剂盒) 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 (显示 TP53 ELISA试剂盒)-independent pathway dependant on Notch1 (显示 NOTCH1 ELISA试剂盒) ubiquitination and proteasome degradation.
These findings suggest that Mdm2 splice isoforms may play critical roles in the regulatory loop of p53 (显示 TP53 ELISA试剂盒)/Mdm2-Mdm4 (显示 MDM4 ELISA试剂盒) via a RING domain-mediated biochemical mechanism.
both MDM2 and MDMX (显示 MDM4 ELISA试剂盒) deletion-caused pancreatic defects are completely rescued by loss of p53 (显示 TP53 ELISA试剂盒), verifying the crucial role of the MDM2 and/or MDMX (显示 MDM4 ELISA试剂盒) in regulating p53 (显示 TP53 ELISA试剂盒) 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
, double minute 2 protein
, p53-binding protein Mdm2