Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

ABSTRACT: The p53 inhibitor MDMX is overexpressed in the vast majority of patients with acute myeloid leukemia (AML). Utilizing hematopoietic stem cells from four non-leukemic/pre-leukemic murine models, we performed bulk transcriptomic analysis to evaluate the impact of Mdmx overexpression.

ORGANISM(S): Mus musculus

PROVIDER: GSE164838 | GEO | 2021/01/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

Project description:MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

| PRJNA692186 | ENA

Effect of depletion of MDMX (aka MDM4) on gene expression in uveal melanoma cell line MEL202

Project description:To investigate the effect of MDMX depletion on the transcriptome of MEL202 cells we established 5 derivatives either containing a doxycyline- inducible Contrl shRNA or with 4 distinct MDMX -targeting shRNAs In thee biological replicates the cells were treated with doxycycline for 48 hrs after which RNA was isolated

2022-08-25 | GSE211802 | GEO

Identification of gene expression changes in MEF cell lines with a targeted MDMX mutation that disrupts binding to CK1-alpha kinase

Project description:The goal of this experiment is to identify genes differentially expressed in MEF cell lines with a targeted MDMX mutation that prevents binding and inhibition of CK1-alpha kinase.

2020-04-07 | GSE148138 | GEO

Microarray of MDMX C462A and wildtype mice treated with acetaminophen

Project description:Microarray of MDMX C462A and wildtype mice treated with acetaminophen

| PRJNA655235 | ENA

scRNA-Seq of MDMX C462A and wildtype mice treated with acetaminophen

Project description:scRNA-Seq of MDMX C462A and wildtype mice treated with acetaminophen

| PRJNA655236 | ENA

Next Generation Sequencing based on the DNA fragment pulled down by p53 antibody (Santa Cruz, sc-126) from MCF7 wile type and MCF7 MDMX-C463A/WT cells.

Project description:Hypothesis: Based on gene chip results and further investigation, MDMX C463A/WT cells shows large portion of transcripts change at p53 dependent manner. As transcriptional factor, p53 regulates those genes could be related to DNA binding status change. ChIP-seq was used to test this hypothesis and figure out global map of p53 binding in MCF7 C463A/WT MCF7 cells by using MCF7 parental cells as reference.

2018-01-24 | GSE109481 | GEO

Proteomic studies of human placentas reveal partnerships associated with preeclampsia, diabetes, gravidity, and labor

Project description:VEGFR2 (Vascular endothelial growth factor receptor 2) is a central regulator of placental angiogenesis. The study of the VEGFR2 proteome of chorionic villi at term revealed its partners MDMX (Double minute 4 protein) and PICALM (Phosphatidylinositol-binding clathrin assembly protein). Subsequently, the oxytocin receptor (OT-R) and vasopressin V1aR receptor were detected in MDMX and PICALM immunoprecipitations. Immunogold electron microscopy showed VEGFR2 on endothelial cell (EC) nuclei, mitochondria, and Hofbauer cells (HC), tissue-resident macrophages of the placenta. MDMX, PICALM, and V1aR were located on EC plasma membranes, nuclei, and HC nuclei. Unexpectedly, PICALM and OT-R were detected on EC projections into the fetal lumen and OT-R on 20-150 nm clusters therein, prompting the hypothesis that placental exosomes transport OT-R to the fetus and across the blood-brain barrier. Insights on gestational complications were gained by univariable and multivariable regression analyses associating preeclampsia with lower MDMX protein levels in membrane extracts of chorionic villi, and lower MDMX, PICALM, OT-R, and V1aR with spontaneous vaginal deliveries compared to cesarean deliveries before the onset of labor. We found select associations between higher MDMX, PICALM, OT-R protein levels and either gravidity, diabetes, BMI, maternal age, or neonatal weight, and correlations only between PICALM-OT-R (p<2.7x10-8), PICALM-V1aR (p<0.006), and OT-R-V1aR (p<0.001). These results offer for exploration new partnerships in metabolic networks, tissue-resident immunity, and labor, notably for HC that predominantly express MDMX.

2024-05-22 | PXD050049 | Pride

Molecular mechanism of CCDC106 regulating the p53-Mdm2/MdmX signaling axis.

Project description:The tumor suppressor p53 (p53) is regulated by murine double minute 2 (Mdm2) and its homologous MdmX in maintaining the basal level of p53. Overexpressed Mdm2/MdmX inhibits cellular p53 activity, which is highly relevant to cancer occurrence. Coiled-coil domain-containing protein 106 (CCDC106) has been identified as a p53-interacting partner. However, the molecular mechanism of the p53/Mdm2/MdmX/CCDC106 interactions is still elusive. Here, we show that CCDC106 functions as a signaling regulator of the p53-Mdm2/MdmX axis. We identified that CCDC106 directly interacts with the p53 transactivation domain by competing with Mdm2 and MdmX. CCDC106 overexpression downregulates the cellular level of p53 and Mdm2/MdmX, and decreased p53 reversibly downregulates the cellular level of CCDC106. Our work provides a molecular mechanism by which CCDC106 regulates the cellular levels of p53 and Mdm2/MdmX.

| S-EPMC10713525 | biostudies-literature

Progression from the preleukemic stage to acute leukemia in TAL1/SCL-LMO1 transgenic mice

Project description:The TAL1/SCL and LMO1 oncogenic transcription factors establish a pre-leukemic state by reprogramming thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Pre-TCR signaling accelerates the progression to T-cell acute lymphoblastic leukemia (T-ALL). To directly address the importance of pre-TCR signaling in driving progression to T-ALL, we leverage on Cd3-deficient mice in which pre-TCR signaling and progression through β-selection is abrogated. In the absence of pre-TCR signaling in Cd3ε-deficient SCL-LMO1 transgenic mice, T-ALL onset is delayed by 150 days. Despite the absence of pre-TCR/CD3 signaling in these mice, we show that leukemic thymocytes exhibit the gene expression profiles of thymocytes that have undergone β-selection, i.e. exhibiting a re-activation of pre-TCR-driven proliferation signature, and a down regulation of HEB/TCF12 target genes. Lastly, monoallelic deletion of Heb is sufficient to accelerate T-ALL onset in Cd3ε-deficient SCL-LMO1 transgenic mice. Together, these results underscore the role of HEB/TCF12 as a tumor suppressor in T-ALL.

2022-03-27 | GSE198506 | GEO

A Novel Cardiotoxic Mechanism for a Pervasive Global Pollutant.

Project description:The Deepwater Horizon disaster drew global attention to the toxicity of crude oil and the potential for adverse health effects amongst marine life and spill responders in the northern Gulf of Mexico. The blowout released complex mixtures of polycyclic aromatic hydrocarbons (PAHs) into critical pelagic spawning habitats for tunas, billfishes, and other ecologically important top predators. Crude oil disrupts cardiac function and has been associated with heart malformations in developing fish. However, the precise identity of cardiotoxic PAHs, and the mechanisms underlying contractile dysfunction are not known. Here we show that phenanthrene, a PAH with a benzene 3-ring structure, is the key moiety disrupting the physiology of heart muscle cells. Phenanthrene is a ubiquitous pollutant in water and air, and the cellular targets for this compound are highly conserved across vertebrates. Our findings therefore suggest that phenanthrene may be a major worldwide cause of vertebrate cardiac dysfunction.

| S-EPMC5282528 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data