MDM2, an introduction.
MDM2 and prognosis.
Mdm2 in evolution.
The 3 best characterized are Mdm2-A, Mdm2-B, and Mdm2-C.
The contribution of the acidic domain of MDM2 to p53 and MDM2 stability.
Binding of an inhibitor of the p53/MDM2 interaction to MDM2.
ARF participates in the regulation of mdm2-p53 pathway by mdm2.
The p53 Arg72Pro and MDM2 -309 polymorphisms and risk of breast cancer in the nurses' health studies.
The -309 SNP in MDM2 is associated with increased MDM2 transcription.
Antisense-MDM2 sensitizes LNCaP prostate cancer cells to androgen deprivation, radiation, and the combination in vivo.
Expression of MDM2 was significantly reduced by AS-MDM2 in the setting of RT.
The polyubiquitination activity of Mdm2/MdmX is Mdm2-dependent.
miR-17-5p/20a are important markers for gastric cancer and murine double minute 2 participates in their functional regulation.
MDM2 restoration by pCMV-MDM2 rescued the functionality.
The MDM2 gene amplification database.
In no case was MDM2 amplification present.
The mdm2 proto-oncogene.
TP53 mutations, amplification of P63 and expression of cell cycle proteins in squamous cell carcinoma of the oesophagus from a low incidence area in Western Europe.
No amplification of MDM2 was found.
Damage-mediated phosphorylation of human p53 threonine 18 through a cascade mediated by a casein 1-like kinase. Effect on Mdm2 binding.
Effect on Mdm2 binding.
Facilitation of adenoviral wild-type p53-induced apoptotic cell death by overexpression of p33(ING1) in T.Tn human esophageal carcinoma cells.
A role for Mdm2 in this synergism is suggested.
Hdmx stabilizes Mdm2 and p53.
[Expression of P21 WAF1/CIP1 in human astrocytomas in correlating with P53, MDM2, and cellular proliferation index].
But not with P53 expression and MDM2 expression.
MDM2: life without p53.
p53 expression in CMV-infected cells: association with the alternative expression of the p53 transactivated genes p21/WAF1 and MDM2.
MDM2+ protein expression.
Analysis of the degradation function of Mdm2.
Functions of the MDM2 oncoprotein.
Defect in the p53-Mdm2 autoregulatory loop resulting from inactivation of TAF(II)250 in cell cycle mutant tsBN462 cells.
These effects of Mdm2 are mediated by p53.
MDM2 overexpression was a rare event.
Mdm2: the ups and downs.
The organization and expression of the mdm2 gene.
Linkage studies in a Li-Fraumeni family with increased expression of p53 protein but no germline mutation in p53.
Therefore MDM2 could be excluded.
MDM2 and p53: a question of balance.
Wild-type p53 differentially affects tumorigenic and metastatic potential of murine metastatic cell variants.
The expression of mdm2 gene was evaluated.
Regulation of p53 stability by Mdm2.
[Tumorogenesis and mdm2 protein].
Mdm2-SUMO1: is bigger better?
Mdm2 in the response to radiation.
Mdmx and Mdm2: brothers in arms?
The MDM2-p53 interaction.
Accumulation of MDM2 in pleomorphic xanthoastrocytomas.
p53 ubiquitination: Mdm2 and beyond.
B1R does not phosphorylate Mdm2.
p53-independent functions of MDM2.
The p53 and Mdm2 families in cancer.
Mdm2 in growth signaling and cancer.
Posttranslational modification of MDM2.
Intrasteric regulation of MDM2.
No tumor had MDM2 amplification.
Mdm2: p53's lifesaver?
MDM2 inhibitors for cancer therapy.
No MDM2 gene amplification was detected.
MDM2 is a negative regulator of p53.
ERK and MDM2 prey on FOXO3a.
MDM2 was not detected in the nucleoli.
The p53 mRNA-Mdm2 interaction.
p53 and Mdm2: an auld alliance.
Targeting MDM2 and MDMX in retinoblastoma.
MDM2 as a predictor of prostate carcinoma outcome: an analysis of Radiation Therapy Oncology Group Protocol 8610.
The intensity of MDM2 staining was not significant.
Mdm2 widens its repertoire.
To confirm it, HEK293 cells were transfected with human HA-MDM2 (+MDM2) or siRNA to MDM2 (-MDM2).
The relationship between MDM2 expression and tumor thickness and invasion in primary cutaneous malignant melanoma.
The rate of MDM2 positivity was 28.9%.
The MDM2-p53 pathway revisited.
Detection of P53 and Mdm2 in vitiligo.
P53 mdm2 inhibitors.
MDM2 as a modifier gene in retinoblastoma.
MDM2 is a negative regulator of p53.
The molecular dynamics of MDM2.
MDM2 and MDMX in cancer and development.
The evolution of MDM2 family genes.
A CD117 and CD34 immunoreactive sarcoma masquerading as a gastrointestinal stromal tumor: diagnostic pitfalls of ancillary studies in sarcoma.
MDM2+ sarcoma is not diagnostic for liposarcoma.
Resistance acquisition to MDM2 inhibitors.
Cardiac sarcoma with MDM2 amplification.
Splice variants of MDM2 in oncogenesis.
MDM2's social network.
Staining for MDM2 and CDK4 was negative.
Mdm2 is an important regulator of p53.
p53-independent effects of Mdm2.
The MDM2 gene family.
p300/MDM2 complexes participate in MDM2-mediated p53 degradation.
[Study on MDM2 and p53 gene proteins expression on acute leukemic cells and its correlation with chemotherapeutic efficacy].
Two of 4 patients with MDM2+++ gained CR and then MDM2 turned negative.
ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways.
We show here that ARF binds to MDM2 and promotes the rapid degradation of MDM2.
The MDM2 C-terminal region binds to TAFII250 and is required for MDM2 regulation of the cyclin A promoter.
There is a positive correlation between MDM2 binding to TAFII250 and MDM2 activation of the cyclin A promoter.
No evidence of MDM2 gene amplification or rearrangement accounting for such an increase in MDM2 expression was found.
Mdm2 levels must be regulated tightly because overexpression of mdm2 contributes to tumorigenesis.
p53 mediated death of cells overexpressing MDM2 by an inhibitor of MDM2 interaction with p53.
p76(MDM2) inhibits the ability of p90(MDM2) to destabilize p53.
Cocompartmentalization of p53 and Mdm2 is a major determinant for Mdm2-mediated degradation of p53.
The Mdm-2 amino terminus is required for Mdm2 binding and SUMO-1 conjugation by the E2 SUMO-1 conjugating enzyme Ubc9.
Because of the biological implication of Mdm2 sumoylation, we mapped Ubc9 binding on Mdm2.
Genetic analysis of the human oncoprotein MDM2 in benign and malignant tumors of the salivary gland.
Correlation between levels of MDM2 mRNA and MDM2 protein could not be detected in the specimens.
Association of p19(ARF) with Mdm2 inhibits ubiquitin ligase activity of Mdm2 for tumor suppressor p53.
The point mutants, which cannot bind to Mdm2, are not ubiquitinated by Mdm2.
mdm2 gene alterations and mdm2 protein expression in breast carcinomas.
p53 expression was associated neither with mdm2 gene amplification nor with mdm2 immunoreactivity.
MDM2-TBP interaction suggests a p53-independent, transcription regulatory role of MDM2.
Overexpression of Mdm2 in mice reveals a p53-independent role for Mdm2 in tumorigenesis.
Mdm2 induced by activated Raf degrades p53 in the absence of the Mdm2 inhibitor p19ARF.
Mdm2 gene amplification in gastric cancer correlation with expression of Mdm2 protein and p53 alterations.
The mdm2 oncogene was amplified by nonradioactive hybridization of tumor DNA with an mdm2 cDNA probe.
MDM2 is under the transcriptional control of p53, and MDM2 acts as a negative regulator of p53.
Progesterone inhibition of MDM2 p90 protein in MCF-7 human breast cancer cell line is dependent on p53 levels.
MDM2 p90 (usually considered to be the major MDM2 protein) binds to and inactivates P53.
MDM2 facilitates p21 degradation independent of ubiquitination and the E3 ligase function of MDM2.
Several spliced forms of MDM2 have been detected in cells that overexpress MDM2.
E2 significantly decreased the stability of p90(MDM2) and p60(MDM2) in MCF-7.
Mdm2 is itself modified with NEDD8 with very similar characteristics to the autoubiquitination activity of Mdm2.