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

p53 and E2F-1 cooperate to mediate apoptosis

X Wu1, A J Levine

  • 1Department of Molecular Biology, Princeton University, NJ 08544-1014.

Proceedings of the National Academy of Sciences of the United States of America
|April 26, 1994
PubMed
Summary

The tumor suppressor p53 and E2F-1 interact in the cell cycle. Coexpression of wild-type p53 and E2F-1 triggers apoptosis, highlighting a critical pathway in cell cycle regulation.

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

Author Correction: Universal DNA methylation age across mammalian tissues.

Nature aging·2023
Same author

Universal DNA methylation age across mammalian tissues.

Nature aging·2023
Same author

Spatial distributions of pericellular stiffness in natural extracellular matrices are dependent on cell-mediated proteolysis and contractility.

Acta biomaterialia·2017
Same author

The association between physical activity and cognition in men with and without HIV infection.

HIV medicine·2017
Same author

The p53 tetramer shows an induced-fit interaction of the C-terminal domain with the DNA-binding domain.

Oncogene·2015
Same author

Involvement of tumor suppressors PTEN and p53 in the formation of multiple subtypes of liposarcoma.

Cell death and differentiation·2015

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The tumor-suppressor protein p53 acts as a G1 checkpoint, responding to DNA damage.
  • Mutations in the p53 gene are linked to genomic instability and cancer.
  • E2F-1, a partner of RB, regulates entry into S phase.

Purpose of the Study:

  • To investigate the potential interactions between p53 and E2F-1 within the cell cycle.
  • To understand how these proteins communicate and influence cell fate.

Main Methods:

  • A human E2F-1 expression plasmid was introduced into murine cells.
  • These cells contained a temperature-sensitive p53 allele, allowing for controlled wild-type and mutant p53 expression.
  • Coexpression of wild-type p53 and E2F-1 was analyzed.

Main Results:

  • Coexpression of wild-type p53 and E2F-1 led to a rapid decrease in cell viability.
  • This loss of viability occurred through apoptosis (programmed cell death).

Conclusions:

  • The cell cycle involves an interactive pathway between the RB-E2F-1 complex and p53.
  • This interaction is crucial for maintaining genomic stability and preventing uncontrolled cell proliferation.

Related Experiment Videos