| Beta-arrestin 2 functions as a G-protein-coupled receptor-activated regulator of oncoprotein Mdm2. | None |
| Ubiquitination and degradation of p53 are largely controlled by Mdm2, an oncogenic E3 ligase. | None |
| Antisense oligonucleotide inhibitors of MDM2 oncogene expression. | None |
| The two upstream open reading frames of oncogene mdm2 have different translational regulatory properties. | None |
| two upstream open reading frames of oncogene mdm2 may play a fundamental role in regulating expression of the mdm2 gene | None |
| Results imply that the current paradigm for understanding Mdm2 action during oncogenesis is incomplete, and its splice variants contribute to human cancer. | None |
| Ribosomal protein L11 negatively regulates oncoprotein MDM2 and mediates a p53-dependent ribosomal-stress checkpoint pathway. | None |
| Cell cycle regulatory functions of the human oncoprotein MDM2. | None |
| Pathobiology of hemophilic synovitis I: overexpression of mdm2 oncogene. | None |
| mdm2 oncogene is overexpressed in hemophilic synovitis I | None |
| Amplification and overexpression of oncogene Mdm2 and orphan receptor gene Nr1h4 in immortal PRKDC knockout cells. | None |
| Genomic organisation of the human MDM2 oncogene and relationship to its alternatively spliced mRNAs. | None |
| The mdm-2 oncogene product forms a complex with the p53 protein and inhibits p53-mediated transactivation. | None |
| MDM2 has oncogenic transformational activities independent of p53--REVIEW | None |
| MDM2 and human malignancies: expression, clinical pathology, prognostic markers, and implications for chemotherapy. | None |
| MDM2 oncogene is overexpressed in more than forty different types of malignancies--REVIEW | None |
| Small molecule antagonists of the MDM2 oncoprotein as anticancer agents. | None |
| MEK-ERK signaling controls Hdm2 oncoprotein expression by regulating hdm2 mRNA export to the cytoplasm. | None |
| The overexpression of MDM2 oncogene related to the poor status and poor prognosis of patients with childhood NHL,correlated with B status and the involved extranodal sites and the increased serum LDH level | None |
| The growth arrest function of the human oncoprotein mouse double minute-2 is disabled by downstream mutation in cancer cells. | None |