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

E2F and Ras synergize in transcriptionally activating p14ARF expression.

Eli Berkovich1, Yocheved Lamed, Doron Ginsberg

  • 1Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovat, Israel.

Cell Cycle (Georgetown, Tex.)
|April 16, 2003
PubMed
Summary

Oncogenic Ras and E2F1 synergize to activate the tumor suppressor p14ARF, even through non-canonical binding sites. This complex regulation of p14ARF highlights its role in cancer. Keywords: p14ARF, tumor suppressor, oncogenic Ras, E2F1.

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

Editorial Expression of Concern: ATM is a target for positive regulation by E2F-1.

Oncogene·2025
Same author

The lincRNA JUNI regulates the stress-dependent induction of c-Jun, cellular migration and survival through the modulation of the DUSP14-JNK axis.

Oncogene·2024
Same author

Correction: The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells.

Oncotarget·2021
Same author

A novel E2F1-regulated lncRNA, LAPAS1, is required for S phase progression and cell proliferation.

Oncotarget·2021
Same author

Theileria parasites subvert E2F signaling to stimulate leukocyte proliferation.

Scientific reports·2020
Same author

In Vitro Evaluation of Chemically Analyzed <i>Hypericum Triquetrifolium</i> Extract Efficacy in Apoptosis Induction and Cell Cycle Arrest of the HCT-116 Colon Cancer Cell Line.

Molecules (Basel, Switzerland)·2019

Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Biology

Background:

  • The INK4a/ARF locus encodes tumor suppressors p16INK4a and ARF, crucial for preventing cancer.
  • ARF regulates the p53 pathway by inhibiting mdm2 and also suppresses proliferation independently of p53.
  • ARF expression is induced by oncogenic stimuli like E2F1.

Purpose of the Study:

  • To investigate the regulation of p14ARF expression by oncogenic Ras and E2F1.
  • To understand the synergistic effects of Ras and E2F1 on p14ARF activation.
  • To explore the mechanisms of p14ARF promoter activation, including non-canonical pathways.

Main Methods:

  • Analysis of p14ARF expression in human cells under oncogenic stimuli.
  • Reporter assays to study p14ARF promoter activity.

Related Experiment Videos

  • Investigation of E2F-binding sites and transcription factor requirements (E2F, Sp-1).

    • Main Results:

    • Oncogenic Ras activates p14ARF in cells with deregulated E2F, but not in normal cells.
    • Oncogenic Ras and E2F1 exhibit synergy in activating p14ARF expression.
    • p14ARF promoter activation by E2F1 occurs via both canonical and non-canonical binding sites.
    • Ras-mediated activation requires both E2F and Sp-1 transcription factors.

    Conclusions:

    • The regulation of the tumor suppressor p14ARF is complex and involves the interplay of oncogenic Ras, E2F1, and Sp-1.
    • Synergistic activation of p14ARF by oncogenic stimuli suggests a critical role in tumor suppression.
    • Non-canonical promoter activation pathways contribute to the intricate control of p14ARF expression.