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-1 induced apoptosis.

A C Phillips1, K H Vousden

  • 1Regulation of Cell Growth Laboratory, NCI-FCRDC, Frederick, MD 21702-1201, USA.

Apoptosis : an International Journal on Programmed Cell Death
|June 5, 2001
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

Cardiovascular reactivity patterns and pathways to hypertension: a multivariate cluster analysis.

Journal of human hypertension·2016
Same author

p53- and p73-independent activation of TIGAR expression in vivo.

Cell death & disease·2015
Same author

Functional interplay between MDM2, p63/p73 and mutant p53.

Oncogene·2014
Same author

Endogenous c-Myc is essential for p53-induced apoptosis in response to DNA damage in vivo.

Cell death and differentiation·2014
Same author

Suppression of acetate mutants in Coprinus : I. Identification of two isoaccepting tRNA suppressors of a missense mutation.

Current genetics·2013
Same author

Suppression of acetate mutants in Coprinus : II. Correlation of recessiveness and dosage effects with suppressed enzyme level.

Current genetics·2013
Same journal

Taginostat, a new quinolone-based HDAC6 inhibitor, promotes apoptosis of chronic lymphocytic leukemia cells in vitro and in vivo by activating STAT4.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Correction: Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Microglial tunneling nanotubes: an intercellular transfer facilitating mitochondrial dysfunction and neuroinflammation in experimental cerebral malaria.

Apoptosis : an international journal on programmed cell death·2026
Same journal

Copper dysregulation in cardiometabolic disease: copper deficiency versus cuproptosis.

Apoptosis : an international journal on programmed cell death·2026
Same journal

GPx6 downregulation drives ferroptosis in Kashin-Beck disease chondrocytes via the SLC7A11/GPx4 axis.

Apoptosis : an international journal on programmed cell death·2026
See all related articles

E2F-1 transcription factor regulates cell cycle and apoptosis by stabilizing p53. This suggests E2F-1 acts as a tumor surveillance mechanism, preventing cancer by initiating cell death in response to abnormal cell growth.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Cycle Regulation

Background:

  • E2F transcription factors are crucial for cell cycle control.
  • Dysregulated E2F activity is common in human cancers.
  • E2F-1's role extends beyond proliferation to include apoptosis regulation.

Purpose of the Study:

  • To investigate the role of E2F-1 in tumor surveillance.
  • To understand how E2F-1 influences apoptosis and proliferation.
  • To explore the interaction between E2F-1 and the p53 tumor suppressor.

Main Methods:

  • Analysis of E2F-1's function in cell cycle regulation.
  • Investigating E2F-1's impact on apoptosis pathways.
  • Studying the stabilization of p53 by E2F-1.

Related Experiment Videos

Main Results:

  • E2F-1 regulates both cell proliferation and apoptosis.
  • E2F-1 stabilizes the p53 tumor suppressor protein.
  • This stabilization is a key mechanism mediating E2F-1's apoptotic function.

Conclusions:

  • E2F-1 functions as a critical component of tumor surveillance.
  • By inducing apoptosis via p53 stabilization, E2F-1 helps prevent tumor formation.
  • E2F-1 represents a potential therapeutic target for cancer treatment.