Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

MdmX represses E2F1 transactivation.

Mark Wunderlich1, Mithua Ghosh, Karen Weghorst

  • 1Wright State University, Department of Biochemistry & Molecular Biology, Dayton, Ohio 45435, USA.

Cell Cycle (Georgetown, Tex.)
|January 24, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Targeting the METTL1/m7G axis as a therapeutic strategy in myeloid leukemia.

Blood·2026
Same author

Combining menin and MEK inhibition to target poor prognosis KMT2A-rearranged RAS pathway-mutant acute myeloid leukemia.

Blood advances·2026
Same author

Development of hematopoietic stem cell-targeted lipid nanoparticles through lipid composition optimization.

Experimental hematology·2026
Same author

Synergistic targeting of eIF4A-mediated translation initiation and apoptosis in acute myeloid leukemia.

Blood neoplasia·2026
Same author

Identifying targeted therapies for CBFA2T3::GLIS2 acute myeloid leukemia.

Leukemia·2026
Same author

Ontogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric Leukemia.

Cancer discovery·2025
Same journal

ALDH18A1 fuels spermine biosynthesis to sustain ferroptosis resistance in cancer and ischemia-reperfusion injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.

Cell cycle (Georgetown, Tex.)·2026
Same journal

OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.

Cell cycle (Georgetown, Tex.)·2026
See all related articles

MdmX protein inhibits E2F1 transactivation independently of p53 and Mdm2. This novel function, mediated by MdmX

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Mdm2 and MdmX are known regulators of the p53 tumor suppressor protein, particularly during early development.
  • Both Mdm2 and MdmX have been implicated in oncogenic activities, and studies suggest they possess p53-independent functions.

Purpose of the Study:

  • To investigate the effect of Mdm2 overexpression on E2F1 transactivation.
  • To uncover novel functions of MdmX, specifically its role in regulating E2F1 transactivation.

Main Methods:

  • Utilized knockout mouse studies to understand Mdm2 and MdmX roles.
  • Employed a series of MdmX deletion mutants to identify the repressive domain.
  • Analyzed E2F1 transactivation in cells overexpressing Mdm2 and MdmX.

Related Experiment Videos

Main Results:

  • Discovered a novel MdmX function: inhibition of E2F1 transactivation, independent of p53 and Mdm2.
  • Identified amino acids 128-444 of MdmX as the repressive domain.
  • Observed a slight reduction in DP1 and increased cytoplasmic localization of E2F1 in MdmX-overexpressing cells, without direct in vivo association.

Conclusions:

  • Elevated MdmX expression can repress E2F1-regulated genes, such as p14ARF.
  • This suggests MdmX acts as a regulatory mechanism within the Rb-p53 signaling pathway, independent of its canonical p53 interactions.