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

Repression of RAD51 gene expression by E2F4/p130 complexes in hypoxia.

R S Bindra1, P M Glazer

  • 1Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520-8040, USA.

Oncogene
|September 27, 2006
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

Systemic delivery of triplex-forming PNA and donor DNA by nanoparticles mediates site-specific genome editing of human hematopoietic cells in vivo.

Gene therapy·2012
Same author

Directed gene modification via triple helix formation.

Current molecular medicine·2002
Same author

Intracellular generation of single-stranded DNA for chromosomal triplex formation and induced recombination.

Nucleic acids research·2002
Same author

Genomic instability in cancer.

Novartis Foundation symposium·2001
Same author

Triplex forming oligonucleotides: sequence-specific tools for gene targeting.

Human molecular genetics·2001
Same author

Gene targeting via triple-helix formation.

Progress in nucleic acid research and molecular biology·2001
Same journal

Aberrant splicing in human cancer shows possible functional impact on transcription factors.

Oncogene·2026
Same journal

The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.

Oncogene·2026
Same journal

Correction: Neuropilin-1 promotes human glioma progression through potentiating the activity of the HGF/SF autocrine pathway.

Oncogene·2026
Same journal

Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene·2026
Same journal

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

Oncogene·2026
Same journal

Correction: SIRT7 activates p53 by enhancing PCAF-mediated MDM2 degradation to arrest the cell cycle.

Oncogene·2026
See all related articles

Hypoxia downregulates DNA repair genes RAD51 and BRCA1 via repressive E2F4/p130 complexes. This coordinated response explains tumor genetic instability and may inform new cancer therapies.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • Dysregulation of DNA repair pathways contributes to hypoxia-induced genetic instability in tumors.
  • Expression of key DNA repair genes like RAD51, BRCA1, MLH1, and MSH2 decreases under hypoxic stress.

Purpose of the Study:

  • To elucidate the mechanistic basis for the hypoxia-induced downregulation of DNA repair genes.
  • To investigate the role of E2F4/p130 complexes in regulating RAD51 and BRCA1 expression under hypoxia.

Main Methods:

  • Analysis of gene expression changes in response to hypoxic stress.
  • Chromatin immunoprecipitation assays to assess protein-DNA interactions at gene promoters.
  • Studies on protein dephosphorylation and nuclear localization.

Related Experiment Videos

Main Results:

  • Hypoxia specifically downregulates RAD51 expression through repressive E2F4/p130 complexes binding to the gene's promoter.
  • A conserved E2F site in the BRCA1 promoter suggests similar regulation.
  • Hypoxia induces p130 dephosphorylation and nuclear accumulation, forming E2F4/p130 complexes that bind RAD51 and BRCA1 promoters.

Conclusions:

  • A coordinated transcriptional program involving repressive E2F4/p130 complexes is integral to the cellular response to hypoxic stress.
  • This co-regulation of homology-dependent DNA repair factors contributes to tumor genetic instability.
  • Findings may guide the development of novel cancer therapeutic strategies.