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

The ARF/p53 pathway.

C J Sherr1, J D Weber

  • 1Department of Tumor Cell Biology, Howard Hughes Medical Institute, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. sherr@stjude.org.

Current Opinion in Genetics & Development
|February 19, 2000
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

The ARF tumor-suppressor controls Drosha translation to prevent Ras-driven transformation.

Oncogene·2013
Same author

Identification of FUSE-binding protein 1 as a regulatory mRNA-binding protein that represses nucleophosmin translation.

Oncogene·2010
Same author

Nucleophosmin protein expression level, but not threonine 198 phosphorylation, is essential in growth and proliferation.

Oncogene·2009
Same author

The INK4-ARF (CDKN2A/B) locus in hematopoiesis and BCR-ABL-induced leukemias.

Cold Spring Harbor symposia on quantitative biology·2008
Same author

Mammalian target of rapamycin: master regulator of cell growth in the nervous system.

Histology and histopathology·2007
Same author

p53-Dependent and -independent functions of the Arf tumor suppressor.

Cold Spring Harbor symposia on quantitative biology·2006
Same journal

Temporal trajectories underlying adult neuronal diversity.

Current opinion in genetics & development·2026
Same journal

Transcription regulation of cell fate plasticity - from embryonic development to tissue regeneration.

Current opinion in genetics & development·2026
Same journal

Shared molecular and cellular programs during regeneration of glandular epithelia.

Current opinion in genetics & development·2026
Same journal

Lineage tracing in human cortical development.

Current opinion in genetics & development·2026
Same journal

Cis-regulatory strategies in developmental patterning.

Current opinion in genetics & development·2026
Same journal

GABAergic neuron fate specification and lineage allocation: from development to disorder.

Current opinion in genetics & development·2026
See all related articles

The ARF tumor suppressor prevents cancer by linking retinoblastoma and p53 pathways. ARF inactivation disrupts p53 function, promoting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • The ARF tumor suppressor is a critical regulator of cell cycle control.
  • ARF links the retinoblastoma protein (Rb) and p53 pathways, both crucial for tumor suppression.
  • Dysregulation of ARF is implicated in various cancers.

Purpose of the Study:

  • To elucidate the role of ARF in connecting Rb and p53 signaling pathways.
  • To understand the mechanism by which ARF inactivation affects p53-dependent apoptosis.
  • To explore the novel function of ARF in regulating p53 stability.

Main Methods:

  • Investigated the interplay between ARF, Rb, and p53.
  • Analyzed p53-dependent apoptosis in response to oncogenic stress.
  • Examined the subcellular localization of Mdm2 in relation to ARF activity.

Related Experiment Videos

Main Results:

  • ARF inactivation was found to reduce p53-dependent apoptosis.
  • ARF promotes the nucleolar relocalization of Mdm2.
  • This relocalization represents a novel mechanism for preventing p53 degradation.

Conclusions:

  • ARF acts as a crucial link between Rb and p53 tumor suppressor pathways.
  • ARF's regulation of Mdm2 localization is key to maintaining p53 stability.
  • Understanding ARF's function provides insights into how stress signals converge to control p53 activity and prevent tumorigenesis.