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

ARF differentially modulates apoptosis induced by E2F1 and Myc.

Jamie L Russell1, John T Powers, Robert J Rounbehler

  • 1Department of Carcinogenesis, Science Park-Research Division, University of Texas M. D. Anderson Cancer Center, Smithville, Texas 78957, USA.

Molecular and Cellular Biology
|February 13, 2002
PubMed
Summary

The tumor suppressor ARF is not required for E2F1-induced apoptosis and actually inhibits E2F1's apoptotic function. Inactivating ARF enhances E2F1's ability to promote apoptosis and cell cycle progression.

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

Insulin Pathway Changes in Localized Prostate Cancer: A Multi-Institutional Analysis.

Cancers·2026
Same author

Improving Provider Awareness and Comfort in Caring for PANDAS in the Outpatient Setting.

Journal of doctoral nursing practice·2026
Same author

Intrinsic tumor factors and extrinsic environmental and social exposures contribute to endometrial cancer recurrence patterns.

Research square·2026
Same author

Global multi-ancestry genome-wide analyses identify genes and biological pathways associated with thyroid cancer and benign thyroid diseases.

Nature genetics·2026
Same author

ShinyEvents: harmonizing longitudinal data for real-world survival estimation.

NPJ precision oncology·2026
Same author

Primary tumor microbiomes predict distant metastasis of colorectal cancer.

NPJ precision oncology·2025

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The ARF tumor suppressor is involved in p53-dependent apoptosis.
  • E2F1 transcription factor promotes proliferation and apoptosis.
  • E2F1 regulates the ARF gene, suggesting ARF's role in E2F1-induced apoptosis.

Purpose of the Study:

  • To investigate the role of ARF in E2F1-induced apoptosis.
  • To determine if ARF is necessary for E2F1 to induce apoptosis.
  • To elucidate the relationship between ARF and E2F1 in vivo and in vitro.

Main Methods:

  • Experiments were conducted in transgenic epidermis in vivo.
  • Studies utilized mouse embryo fibroblast cultures in vitro.
  • Assessed apoptosis induction by E2F1 and Myc in the presence and absence of ARF.

Related Experiment Videos

Main Results:

  • ARF is unnecessary for E2F1-induced apoptosis.
  • Inactivation of ARF enhances E2F1's apoptotic function.
  • ARF inactivation cooperates with E2F1 to promote S-phase entry.
  • E2F1 induces p53 accumulation and phosphorylation in the absence of ARF.
  • Myc-induced apoptosis is diminished without ARF.

Conclusions:

  • ARF acts as a negative regulator of E2F1 activity.
  • ARF is not required for E2F1-mediated apoptosis.
  • The absence of ARF potentiates E2F1's pro-apoptotic and proliferative effects.