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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
Study found significantly higher MDM2 single nucleotide polymorphism 309 GG genotype and G allele frequencies in the Brazilian Li-Fraumeni syndrome cohort than in controls.
Our case-control analysis revealed that MDM2 rs937283 was associated with the susceptibility to breast and liver cancer, but not cervical, colon, or rectal cancer.
Meta-analysis found that significant association between the MDM2 rs2279744 polymorphism and increased retinoblastoma (Rb) risk, while MDM2 rs937283 polymorphism was associated with significantly decreased RB risk. However, as to the P21 rs1801270 polymorphism, a statistically significant association was not identified for RB.
Meta-analysis suggested that MDM2 SNP309 polymorphism increased the risk of endometrial cancer significantly, especially in endometrioid and Type I endometrial cancer, indicating MDM2 could serve as a potential diagnostic factor marker for endometrial cancer.
The Numb-Mdm2 interaction represents a fuzzy complex mediated by a short Numb sequence encompassing its alternatively spliced exon 3 (Ex3), which is necessary and sufficient to inhibit Mdm2 and prevent p53 degradation.
It has been shown that MDM2 and MDMX are targetable vulnerabilities within TP53-wild-type T-cell lymphomas.
MDM2 down-regulation attenuates the senescence-associated secretory phenotype.
First evidence that DNA induction of MDM2 promotes proliferation of human renal mesangial cells and alters peripheral B cells subsets in pediatric systemic lupus erythematosus.
The genotypes of MDM2 SNP309 may allow forr early detection of and predictor for colorectal cancer risk, especially among smokers and non-alcohol drinkers, but not for prognosis.
Our study showed that miR-145 suppressed MDM2 expression, which subsequently influenced the p53-related cell growth pattern in pterygial epithelium. The regulatory miR-145/MDM2-p53 loop can serve as a potential target for treatment of pterygium.
In contrast to other deubiquitinating enzymes (DUBs) that have been previously implicated in the regulation of Mdm2 protein stability, USP48 did not induce Mdm2 stabilization by significantly reducing Mdm2 ubiquitination levels.
MDM2 rs937283 A > G variant is associated with lung and gastric cancer.
No associations were found between MDM2 SNP309 and either of two FSH/LH groups.
MDM2 promoter variants play a role in determining the risk of recurrence of squamous cell carcinoma of oropharynx
In silico molecular docking and dynamics studies with MDM2-p53 protein revealed that HTMF was more potent compound that could inhibit the binding of MDM2 with p53 and, therefore, could trigger apoptosis in cancer cell.
Our findings suggested that RBM38 may be a core contributor in stabilizing the p53-mdm2 loop function to prevent hepatocellular carcinoma (HCC) and a potential novel target to provide a therapeutic strategy for HCC by inhibiting mdm2 and rescuing p53 from inactivation.
As shown in human MDM2-ALT1-expressing p53 null transgenic mice, MDM2-ALT1 can direct rhabdomyosarcoma (RMS) tumor formation recapitulating many of the histological and immunohistochemical features of fusion-negative RMS.
We demonstrate that extraskeletal osteosarcoma (ESOS) may include at least two small subsets: an MDM2-amplified deep soft-tissue ESOS and an H3K27me3-deficient organ-based ESOS
miR-518 acted as a new tumor suppressor by targeting MDM2 gene and trigger apoptosis in vivo and in vitro.
Overexpression of miR-641 decreased the expression of MDM2 and increased the expression of p53 in lung cancer cells.
results suggest overexpression of MDM2 is closely linked to inhibition of p53-dependent apoptosis of Theileria parva-infected lymphocytes; aberrant expression of host lymphocyte MDM2 induced by cytoplasmic existence of T. parva, directly and/or indirectly, is associated with aspects of this type of transformation of T. parva-infected lymphocytes
mutant Mdm2 was unable to rescue a p53-induced apoptotic phenotype.
Data indicate that knockdown of the Mdm2 and Mdm4 caused dramatic accumulation of mutant p53 protein.
Together with p53, provides an experimental model for characterizing drugs and genes that affect p53 signaling.
Data show that liver-specific expression of p53-negative regulator mdm2 leads to growth retardation and fragile liver in zebrafish.
The proximal p53 inhibitor MDM2 is markedly downregulated in subcutaneous white and brown adipose tissues of mice during aging. Genetic disruption of MDM2 in adipocytes triggers canonical p53-mediated apoptotic and senescent programs, leading to age-dependent lipodystrophy and its associated metabolic disorders, including type 2 diabetes, nonalcoholic fatty liver disease, hyperlipidemia, and energy imbalance.
To investigate whether MDM2C462A, which retains p53 binding, has p53-suppressing activity, we generated Mdm2C462A/C462A;p53ER/- mice. Adult Mdm2-null mice died approximately 7 days after tamoxifen-induced p53 activation, indicating that in the absence of MDM2, MDMX cannot suppress p53. p53 activity is higher in the presence of MDM2C462A than in the absence of MDM2.
These results show that ischemic preconditioning increased neuronal MDM2 protein levels, which prevented ischemia-induced p53 stabilization and neuronal death.
the disruption of Mdm2/p53 interaction affects the early-embryonic otic progenitor cells and their descendants.
E2F6 suppresses Mdm2 expression in cells harboring the SNP309G allele but not the SNP309T allele.
the MDM2-p53-PC signalling axis links mitochondrial metabolism to insulin secretion and glucose homeostasis, and could represent a therapeutic target in diabetes.
Selective dysregulation of Mdm2 and Mdm4 alternative splicing underlies p53 anti-repression and motor neuron death in a mouse model of spinal muscular atrophy.
Aging mouse models have revealed the complexity of the p53-Mdm2 axis and have solidly placed the p53 network as being key to many aspects of both pathological aging conditions and normal aging (review).
The results indicated that simultaneously knocking down MDM2 and overexpressing p53 was able to inhibit proliferation and induce G1 cell cycle arrest in H1299 cells, compared with either alone.
These results illustrate the importance of the cooperative activities of p53 and Mdm2 in a network of miRNAs that function to impose a barrier against aberrant cardiomyocyte cell cycle re-entry to maintain cardiac homeostasis.
c-Abl phosphorylation of Mdm2 has a role in regulation of p53 tumor suppression and bone marrow failure
Bre enhances osteoblastic differentiation by promoting the Mdm2-mediated degradation of p53.
genetic and biochemical data support a role for Mdm2 in cardiac growth control through the regulation of p53, the Pgc-1 family of transcriptional coactivators and the pivotal antioxidant Pink1
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-Mdm2 signaling on p53 tumor suppression and reveal that destabilizing Mdm2 by promoting its phosphorylation by ATM would be effective in treating oncogene-induced malignancies.
the existence of an unusual functional interplay between STATs and CREB at the onset of adipogenesis through shared CRTC cofactors, is reported.
Mdm2 expression is required for cell survival even in the absence of p53. Moreover, results suggest that p73 compensates for loss of p53.
In Fmr1 KO neurons, Mdm2 is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 KO. Expression of a dephosphomimetic of Mdm2 rescues PSD-95 ubiquitination, degradation and synapse elimination in Fmr1 KO neurons.
MDM2 is a non-redundant survival factor for proximal tubular cells by protecting them from spontaneous p53 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.
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