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 mediates density-dependent growth arrest.

A Meerson1, M Milyavsky, V Rotter

  • 1Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, Hebrew University, Givat Ram, Jerusalem 91904, Israel.

FEBS Letters
|February 13, 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

Immunophenotypes and Gene Rearrangements of the T-Cell Receptor in Two Patients with a Large Granular Lymphocyte Disorder.

Leukemia & lymphoma·2016
Same author

Novel p53 target genes secreted by the liver are involved in non-cell-autonomous regulation.

Cell death and differentiation·2015
Same author

Modulation of alternative splicing contributes to cancer development: focusing on p53 isoforms, p53β and p53γ.

Cell death and differentiation·2014
Same author

The onset of p53 loss of heterozygosity is differentially induced in various stem cell types and may involve the loss of either allele.

Cell death and differentiation·2014
Same author

Human adipose microRNA-221 is upregulated in obesity and affects fat metabolism downstream of leptin and TNF-α.

Diabetologia·2013
Same author

p53 is required for brown adipogenic differentiation and has a protective role against diet-induced obesity.

Cell death and differentiation·2013
Same journal

Identification of a Shiga toxin A-derived peptide internalized into Gb3 receptor-bearing cells via interaction with the Shiga toxin B subunit.

FEBS letters·2026
Same journal

The dual role of lectins in cancer-immunotherapy tools and therapeutic targets.

FEBS letters·2026
Same journal

Decoding the dynamic extracellular matrix in cancer-3D models and bioscaffolds rewire the rules of tumor progression.

FEBS letters·2026
Same journal

Extending the classical sequence-structure-function paradigm through protein dynamics and context-dependent behavior.

FEBS letters·2026
Same journal

α-Synuclein aggregation landscape from phase separation to neurotoxic intermediates.

FEBS letters·2026
Same journal

Modelling stem cell differentiation related processes-A practical overview for biologists.

FEBS letters·2026
See all related articles

Basal p53 expression in fibroblasts controls cell growth and cycle arrest by regulating p16/INK4a. Loss of this regulation in aged cells leads to uncontrolled growth and p53-dependent cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The tumor suppressor p53 is crucial for stress responses.
  • Emerging evidence links p53 to fundamental cellular behaviors.
  • Its role in normal cell function requires further elucidation.

Purpose of the Study:

  • To investigate the role of basal p53 expression in normal fibroblast behavior.
  • To determine p53's involvement in growth control and cell cycle regulation.
  • To explore p53's function in aged cells exhibiting loss of growth inhibition.

Main Methods:

  • Utilized WI38 human embryonic lung fibroblasts.
  • Assessed basal p53 expression effects on growth rate and cell cycle.
  • Investigated density-dependent regulation of p16/INK4a and p27/KIP.

Related Experiment Videos

  • Analyzed changes in immortalized WI38 cells with prolonged culturing.

    • Main Results:

    • Basal p53 restricts fibroblast growth rate and mediates density-dependent growth inhibition.
    • p53 influences G1 phase arrest via p16/INK4a density-dependent regulation.
    • Aged WI38 cells lose density-dependent growth inhibition.
    • This loss correlates with p27/KIP deregulation and INK4a locus silencing.
    • Prolonged culture induces p53-dependent, contact-induced cell death.

    Conclusions:

    • Basal p53 plays a key role in normal fibroblast growth control and cell cycle regulation.
    • p53's regulation of p16/INK4a is critical for density-dependent inhibition.
    • Cellular aging disrupts p53-mediated growth control, leading to senescence or death.
    • Understanding p53's non-canonical roles is vital for cancer research and aging.