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 mutants suppress ZBP-89 function.

Morihiro Okada1, Arthur Tessier, Longchuan Bai

  • 1Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-2200, USA.

Anticancer Research
|July 11, 2006
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

Investigating machine learning algorithms to classify label-free images of pancreatic neuroendocrine neoplasms.

Biophotonics discovery·2026
Same author

Extracellular signalling regulates gastrin transcription through site-specific phosphorylation and nuclear redistribution of Menin.

bioRxiv : the preprint server for biology·2026
Same author

ZFP148 is a transcriptional repressor of cytolytic effector CD8<sup>+</sup> T cell differentiation.

Nature immunology·2026
Same author

Discovery of SD-965 as a Potent, Selective, and Efficacious STAT3 PROTAC Degrader.

Journal of medicinal chemistry·2026
Same author

BCR::ABL1-Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B-ALL Cells to Enhancer-Targeting Drugs.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms.

Molecular cancer·2026
Same journal

Corrigendum.

Anticancer research·2026
Same journal

Geographic Variation in Stage at Diagnosis of Skin Cancer in the United States: A National Cancer Database Analysis.

Anticancer research·2026
Same journal

Anti-tumor Effects of Loureirin A Treatment in Colorectal Cancer Cells <i>via</i> Inhibition of AKT Phosphorylation.

Anticancer research·2026
Same journal

Bayesian Analysis to Refine East Asian Subgroup Estimates in the CLEAR Trial (Lenvatinib Plus Pembrolizumab <i>vs</i>. Sunitinib) for Advanced Renal Cell Carcinoma.

Anticancer research·2026
Same journal

Pulsed Electromagnetic Field Increases Doxorubicin-induced Mitotic Slippage in MDA-MB-231 Breast Cancer Cells.

Anticancer research·2026
Same journal

Geographic Disparities in Socioeconomic Factors and Advanced-stage Presentation in Rectosigmoid Cancer: A National Cancer Database Analysis.

Anticancer research·2026
See all related articles

Zinc finger protein ZBP-89 acts as a co-activator for wild-type p53. Functionally inactive p53 mutants negatively impact ZBP-89 activity, affecting chemotherapy sensitivity.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Transcription Factors

Background:

  • ZBP-89 is a transcription factor that regulates gene expression and influences apoptosis.
  • Wild-type p53 is a tumor suppressor, and its mutations are linked to cancer development and chemotherapy resistance.

Purpose of the Study:

  • To investigate the interaction between ZBP-89 and various p53 mutants.
  • To determine how ZBP-89 affects chemotherapy sensitivity in cells with wild-type, mutated, or absent p53.

Main Methods:

  • Studied the effect of ZBP-89 on seven sporadic p53 mutants.
  • Assessed chemotherapy sensitivity in p53-null versus p53-mutant cells with altered ZBP-89 levels.

Main Results:

  • ZBP-89 stabilized wild-type p53 but only the A161T p53 mutation showed constitutive activity.

Related Experiment Videos

  • ZBP-89 enhanced p53-mediated cell death with specific chemotherapeutic agents, except for the R273H p53 mutation.
  • Chemotherapy sensitivity varied depending on p53 status and ZBP-89 levels.

    • Conclusions:

    • ZBP-89 functions as a crucial co-activator for wild-type p53.
    • Inactive p53 mutants can disrupt the ZBP-89/p53 pathway, impacting therapeutic outcomes.