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

Regulating the p53 system through ubiquitination.

Yili Yang1, Chou-Chi H Li, Allan M Weissman

  • 1Regulation of Protein Function Laboratory, Center for Cancer Research, National Cancer Institute-Frederick, 1050 Boyles Street, 560/22-64, Frederick, MD 21702, USA. yangyili@ncifcrf.gov

Oncogene
|March 17, 2004
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

Molecular characterization of a rare heterozygous <i>APOA5</i> variant in a Chinese family with moderate hypertriglyceridemia.

Frontiers in genetics·2026
Same author

CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.

Non-coding RNA research·2026
Same author

Comment on "Estimating resting energy expenditure in severely obese patients with laparoscopic sleeve gastrectomy: Normalized lean weight appears to be more accurate: A prospective observational study".

Nutrition (Burbank, Los Angeles County, Calif.)·2026
Same author

Inhalable extracellular vesicles as cell-free therapeutics for chronic respiratory disease.

Frontiers in bioengineering and biotechnology·2026
Same author

Engineered pistol ribozymes selectively target KRAS G12V with enhanced efficacy by capping modification.

Cell chemical biology·2026
Same author

Proof-of-concept bioelectrochemical characterization of Mycolicibacterium smegmatis for diagnostic applications.

Bioelectrochemistry (Amsterdam, Netherlands)·2026
Same journal

SRD5A3-mediated aberrant N-glycosylation of SCARA5 promotes ferroptosis in lung adenocarcinoma.

Oncogene·2026
Same journal

Aberrant splicing in human cancer shows possible functional impact on transcription factors.

Oncogene·2026
Same journal

The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.

Oncogene·2026
Same journal

Correction: Neuropilin-1 promotes human glioma progression through potentiating the activity of the HGF/SF autocrine pathway.

Oncogene·2026
Same journal

Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene·2026
Same journal

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

Oncogene·2026
See all related articles

The tumor suppressor p53 is regulated by ubiquitination. Reactivating p53 by targeting its degradation pathways shows promise for cancer therapy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • The tumor suppressor p53 is crucial for preventing cancer but is typically kept at low levels through constant ubiquitination and proteasomal degradation.
  • Stress responses inhibit p53 ubiquitination, leading to its accumulation and activation, which can induce cell cycle arrest or apoptosis.
  • Defects in the p53 system are common in human tumors, highlighting its importance in cancer development.

Purpose of the Study:

  • To explore targeting p53 ubiquitination as a strategy for cancer treatment.
  • To review the molecular mechanisms regulating p53 ubiquitination and its role in tumor suppression.
  • To identify potential therapeutic approaches for reactivating p53 in cancer cells.

Main Methods:

  • Review of existing literature on p53 ubiquitination and regulation.

Related Experiment Videos

  • Analysis of molecular mechanisms controlling p53 stability and activation.
  • Identification of strategies to inhibit p53 degradation pathways.

    • Main Results:

    • Understanding the molecular mechanisms of p53 ubiquitination has advanced significantly.
    • Inhibiting E3 ligase activity (e.g., Mdm2), blocking p53-Mdm2 interactions, and restoring mutated p53 function are viable strategies.
    • These approaches can selectively lead to the accumulation and activation of p53 in tumor cells.

    Conclusions:

    • Targeting p53 ubiquitination offers a promising avenue for developing novel cancer therapies.
    • Reactivating the p53 pathway by modulating its degradation holds potential for selective tumor cell killing.
    • Future chemotherapeutic agents may be developed based on these insights into p53 regulation.