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

SUMO is growing senescent.

Oliver Bischof1, Anne Dejean

  • 1Unité d'Organisation Nucléaire et Oncogenèse/INSERM U579, Institut Pasteur, Paris, France. obischof@pasteur.fr

Cell Cycle (Georgetown, Tex.)
|March 22, 2007
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

Z-DNA formation regulates the totipotent-like state and primes Zscan4-dependent chromatin compartmentalization.

Nature structural & molecular biology·2026
Same author

Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.

GeroScience·2026
Same author

Chemical inhibition of SUMOylation activates the FSHD locus.

Scientific reports·2026
Same author

SUMO operates from a unique long tandem repeat to keep innate immunity in check.

Nucleic acids research·2025
Same author

[Pierre Tiollais (1934-2024), a pioneer in genetic engineering with a lifelong commitment to the hepatitis B virus].

Medecine sciences : M/S·2025
Same author

Biographical Feature: In memoriam Pierre Tiollais (1934-2024).

Journal of virology·2025
Same journal

ALDH18A1 fuels spermine biosynthesis to sustain ferroptosis resistance in cancer and ischemia-reperfusion injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Circular RNA circ_0001829 attenuates G2/M arrest to promote hepatocyte proliferation by sponging miR-3095-3p following liver injury.

Cell cycle (Georgetown, Tex.)·2026
Same journal

Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.

Cell cycle (Georgetown, Tex.)·2026
Same journal

BMSCs-derived exosomal miR-196a-5p promotes macrophage M2 polarization and osteogenesis in postmenopausal osteoporosis through regulating Rspo2/Wnt/β-catenin signaling.

Cell cycle (Georgetown, Tex.)·2026
Same journal

MicroRNA-6833-3p drives prostate cancer progression and stemness by targeting the NUMB-mediated NOTCH signaling pathway.

Cell cycle (Georgetown, Tex.)·2026
Same journal

OTUD5 promotes AML progression by stabilizing SLC7A11 to suppress ferroptosis.

Cell cycle (Georgetown, Tex.)·2026
See all related articles

Cellular senescence, a key tumor suppressor mechanism, involves the E3 SUMO ligase PIASy. This study reveals SUMOylation

Area of Science:

  • Cellular biology
  • Molecular oncology
  • Biochemistry

Background:

  • Cellular senescence is a vital tumor suppressive mechanism preventing uncontrolled cell proliferation.
  • The role of post-translational modifications in senescence is an emerging area of research.

Purpose of the Study:

  • To investigate the direct involvement of SUMOylation in the senescence program.
  • To explore the function of the E3 SUMO ligase PIASy in cellular senescence.

Main Methods:

  • Investigated the role of PIASy in senescence.
  • Examined the impact of SUMO modification on cell cycle arrest.

Main Results:

  • PIASy, an E3 SUMO ligase, was found to actively contribute to the senescence program.

Related Experiment Videos

  • This provides the first evidence for a direct role of SUMO modification in cellular senescence.
  • Conclusions:

    • SUMOylation, mediated by PIASy, is a direct participant in the execution of cellular senescence.
    • Further research into the SUMO pathway's role in senescence and tumorigenesis is warranted.