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 transactivation through various p53-responsive elements

D J Park1, A M Chumakov, C W Miller

  • 1Division of Hematology/Oncology, Cedars-Sinai Medical Center, University of California-Los Angeles School of Medicine, 90048-0750, USA.

Molecular Carcinogenesis
|June 1, 1996
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

Global Forum of Cancer Surgeons: Cancer Surgery During the COVID-19 Pandemic: Impact and Lessons Learned.

Annals of surgical oncology·2022
Same author

Short-term outcomes of a multicentre randomized clinical trial comparing laparoscopic pylorus-preserving gastrectomy with laparoscopic distal gastrectomy for gastric cancer (the KLASS-04 trial).

The British journal of surgery·2021
Same author

Developmental Nutrition Affects the Structural Integrity of a Sexually Selected Weapon.

Integrative and comparative biology·2021
Same author

Short communication: Dietary bovine milk-derived exosomes improve bone health in an osteoporosis-induced mouse model.

Journal of dairy science·2020
Same author

Electrically controllable THz asymmetric split-loop resonator with an outer square loop based on VO<sub>2</sub>.

Optics express·2018
Same author

Experimental manipulation reveals a trade-off between weapons and testes.

Journal of evolutionary biology·2017
Same journal

Acylglycerol Kinase Sensitizes Glioblastoma to Temozolomide via Limiting Mitochondrial Damage Related Cellular Senescence.

Molecular carcinogenesis·2026
Same journal

Accelerated Biological Aging Increases the Risk of Head and Neck Cancer: Insights From Genetic Instruments of Epigenetic Clocks.

Molecular carcinogenesis·2026
Same journal

Colorectal Cancer Liver Metastasis-Associated Ferroptosis-Related Genes Modulate Lipid Peroxidation in Colorectal Cancer Cells.

Molecular carcinogenesis·2026
Same journal

Ubiquitin Specific Peptidase 48 Deubiquitinates METTL3 to Modulate Ferroptosis in Gastric Cancer Cells.

Molecular carcinogenesis·2026
Same journal

Prevention of Myc-Driven Prostate Cancer in Mice by Oral Administration of Sulforaphane.

Molecular carcinogenesis·2026
Same journal

Association of Expression of YTH-Domain Family Protein 3 (YTHDF3) With Brain Metastases and Unfavorable Survival in Patients With Stage IV Lung Adenocarcinoma.

Molecular carcinogenesis·2026
See all related articles

The p53 tumor suppressor protein

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The p53 protein is a key nuclear phosphoprotein involved in tumor suppression.
  • p53 functions by binding to specific DNA recognition sequences to regulate gene transcription.
  • Identifying and characterizing these recognition sequences is crucial for understanding p53's role.

Purpose of the Study:

  • To compare the transcriptional mediation abilities of different p53 recognition sequences.
  • To assess these abilities in the presence of wild-type (wt) and mutant p53.
  • To investigate the impact of specific p53 mutations on transcriptional activity.

Main Methods:

  • Constructed three p53-responsive chloramphenicol acetyltransferase (CAT) reporter constructs: pOST2, pRGC, and pMCK.

Related Experiment Videos

  • Transfected these constructs into human carcinoma cell lines with varying p53 mutations.
  • Co-transfected cells with wt or mutant p53 expression vectors and measured CAT activity for transactivation.

    • Main Results:

    • pOST2 demonstrated a greater ability to mediate p53-driven transactivation compared to pRGC and pMCK.
    • p53 mutations at codons 175 or 248 abolished transactivation across all tested reporter constructs.
    • pOST2 uniquely mediated transactivation with codon 273-mutant p53, unlike pRGC and pMCK.

    Conclusions:

    • Different p53 recognition sequences exhibit varying sensitivities to specific wild-type and mutant p53 proteins.
    • These differential sensitivities are significant for p53's function as a transcriptional activator.
    • This highlights the importance of p53-responsive elements in normal physiology and carcinogenesis.