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Herein is shown that tumor cells with MDM2 amplification are selectively resistant to treatment with topoisomerase II (show TOP2 ELISA Kits) poisons but not other DNA damaging agents.Herein is shown that tumor cells with MDM2 amplification are selectively resistant to treatment with topoisomerase II (show TOP2 ELISA Kits) poisons but not other DNA damaging agents
MDM2 rs1690916 and rs2279744 cannot be considered as genetic risk factors for osteosarcoma susceptibility in different populations [review and meta-analysis]
The MDM2 T/T genotype was predictive of poorer survival in a Japanese population of lung adenocarcinoma patients.
Blocking the MDM2 protein-XIAP (show XIAP ELISA Kits) mRNA interaction reduces MDM2 and XIAP (show XIAP ELISA Kits) levels and activates p53 (show TP53 ELISA Kits).
Patients with alterations in TP53 (show TP53 ELISA Kits) or MDM2 had a reduced progression-free survival, and TP53 (show TP53 ELISA Kits)/MDM2 alterations were an independent predictor of disease progression after cisplatin-based chemotherapy. TP53 (show TP53 ELISA Kits) alterations were identified in 72% of patients with primary mediastinal nonseminoma, which may explain their inferior outcomes.
our findings indicate the functional role of HBx in regulating the stem-like properties of OV6(+) CSCs in HCC (show FAM126A ELISA Kits) through the MDM2/CXCL12 (show CXCL12 ELISA Kits)/CXCR4 (show CXCR4 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling axis, and identify HBx, MDM2, CXCR4 (show CXCR4 ELISA Kits) and OV6 as a novel prognostic pathway and potential therapeutic targets for patients with HBV-related HCC (show FAM126A ELISA Kits) patients
This study suggests that MDM2 activates Smad (show SMAD1 ELISA Kits) pathway to promote EMT (show ITK ELISA Kits) in ovarian cancer metastasis.
The MDM2 SNP309 in retinal pigment epithelial cells enhances their potential of proliferative vitreoretinopathy pathogenesis.
High MDM2 expression is associated with acute myeloid leukemia (show BCL11A ELISA Kits).
mutant Mdm2 was unable to rescue a p53 (show TP53 ELISA Kits)-induced apoptotic phenotype.
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.
both MDM2 and MDMX (show MDM4 ELISA Kits) deletion-caused pancreatic defects are completely rescued by loss of p53 (show TP53 ELISA Kits), verifying the crucial role of the MDM2 and/or MDMX (show MDM4 ELISA Kits) in regulating p53 (show TP53 ELISA Kits) in a spatio-temporal manner during the development, functional maintenance, and related disease progress of endocrine pancreas.
Vif (show BTG1 ELISA Kits) stabilization by CBFbeta (show CBFB ELISA Kits) is mainly caused by impairing MDM2-mediated degradation.
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