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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
MDM2 Deficiency is associated with chemoresistance in Acute Myeloid Leukemia.
co-immunoprecipitation (CoIP) experiments showed that RRS1 knockdown activated p53 by facilitating the direct contact of MDM2 and RPL11/RPL5. Taken together, our results suggest that RRS1 may contribute to breast cancer proliferation through RPL11/MDM2-mediated p53 activation.
HMGA2 promotes intestinal carcinogenesis by decreasing the stability of the p53 protein and promoting MDM2-mediated p53 ubiquitination and degradation.
MDM2 directly binds and sequesters NDUFS1, preventing its mitochondrial localization and ultimately causing complex I and supercomplex destabilization and inefficiency of oxidative phosphorylation.
reveal a novel role for the MDM2-p53 interaction in neuronal apoptosis after ischemia and show that the MDM2 SNP309 determines the functional outcome of patients after stroke
Describe subcutaneous fatty neoplasm characterized by notable adipocytic size variation, patchy single-cell fat necrosis, focal (usually mild) adipocytic atypia, p53 overexpression, RB1 gene abnormalities and an absence of MDM2 gene amplification.
the time course of Mdm2-p53 dissociation may impact on intracellular proteins involved in cell differentiation fate. These results suggest that the long-lasting Mdm2 binding plays a key role in the mobilization of intracellular proteins that regulate the final biological outcome of MSCs.
The phosphomimetics reduced Mdm2 and MdmX binding affinity by 35-fold, but resulted in minimal changes in transient secondary structure, suggesting that the destabilizing effect of phosphorylation on the p53TAD-Mdm2 interaction is primarily electrostatic.
Mechanistic studies demonstrated that overexpression of Fn14 could reduce the formation of a Mdm2-p53-R248Q-Hsp90 complex by downregulating Hsp90 expression, indicating that degradation of p53-R248Q was accelerated via Mdm2-mediated ubiquitin-proteasomal pathway
Aberrant co-expression of P53 and MDM2 is associated with advanced stage in laryngeal squamous cell carcinoma (LSCC). Furthermore, MDM2 overexpression is a frequent and critical genetic event in LSCC and seems to negatively affect survival.
Study show for the first time that the expression of MDM2 in ERalpha+ breast cancer and triple-negative breast cancer (TNBC) can result in different tumor-promoting outcomes. Both MDMX and MDM2 overexpression in TNBC MDA-MB-231 cells enhanced the circulating tumor cells phenotype. These data indicate that both MDM2 and MDMX can promote TNBC metastasis.
T309G polymorphism might be a low-penetrant risk factor for leukemia among Chinese [meta-analysis]
MDM2-C may have a positive or negative role in breast tumorigenesis depending on mutant tp53 expression
This data extends the earlier mechanisms proposed to rationalize the entropically driven binding of the p53 set and the enthalpically driven binding of the 12/1 set... understanding the conformational landscapes of the MDM2-binding peptides may suggest new peptide designs with bespoke binding mechanisms
Spindlin 1 (SPIN1) sequesters ribosomal protein uL18 in the nucleolus, preventing it from interacting with c-mdm2 Proto-oncogene protein (MDM2), and alleviating uL18-mediated inhibition of MDM2 ubiquitin ligase activity toward p53 tumor suppressor protein (p53).
Results found that the SNP309G-allele in MDM2 promotor region attenuates the p53-response and leads to a higher breast cancer risk, but also to a later onset of breast cancer and a trend towards a good prognosis.
Expression of murine double minute 2 (MDM2) is increased in Endometrial cancer (EC) tissues and cell lines. The EC cells treated with CP31398 or siRNA against MDM2 exhibit an increased apoptosis and a suppressed migration and invasion. Treatment with CP31398 and siRNA against MDM2 further enhance these effects.
Brain-specific angiogenesis inhibitor 1 (BAI1) prevents proto-oncogene Protein c-mdm2 (Mdm2)-mediated tumor supressor p53 (p53) polyubiquitination, and its loss substantially reduces p53 levels.
TRIM65 binds to the N-terminus of p53 tumor suppressor and thus competes with MDM2 for p53 binding.
The study shows complex interrelation between apoptosis and cell cycle regulating proteins (MDM2, BCL2 and Bax) in benign prostatic hyperplasia and prostate cancer.
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.
MCM2 deletion is associated with female infertility.
G protein-coupled receptor family C group 5 member A (GPRC5A) deficiency contributes to dysregulated proto-oncogene protein c-mdm2 (MDM2) via activated epidermal growth factor receptor (EGFR) signaling, which promotes lung tumor development.
MDM2 controls diabetic and non-diabetic renal antioxidant capacity via NRF2. NRF2 predominantly mediates MDM2's action on diabetic kidney disease. P53 is a key factor through which MDM2 activates NRF2 in diabetic kidney disease.
EmicroEBNA1 tumour cells are dependant upon Mdm2 for survival.
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]
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