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

Jab1 is a specificity factor for E2F1-induced apoptosis.

Timothy C Hallstrom1, Joseph R Nevins

  • 1Duke Institute for Genome Sciences and Policy Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.

Genes & Development
|February 17, 2006
PubMed
Summary

Jab1 is a newly identified cofactor essential for E2F1-induced apoptosis. This protein binds E2F1 and synergistically promotes programmed cell death and p53 accumulation, but not cell cycle progression.

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

UHRF2 accumulates in early G<sub>1</sub>-phase after serum stimulation or mitotic exit to extend G<sub>1</sub> and total cell cycle length.

Cell cycle (Georgetown, Tex.)·2024
Same author

UHRF2 regulates cell cycle, epigenetics and gene expression to control the timing of retinal progenitor and ganglion cell differentiation.

Development (Cambridge, England)·2022
Same author

Developmental Iron Deficiency Dysregulates TET Activity and DNA Hydroxymethylation in the Rat Hippocampus and Cerebellum.

Developmental neuroscience·2022
Same author

Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape.

Nutrients·2021
Same author

Retinoblastoma tumor cell proliferation is negatively associated with an immune gene expression signature and increased immune cells.

Laboratory investigation; a journal of technical methods and pathology·2021
Same author

Author Correction: Division of labour between Myc and G1 cyclins in cell cycle commitment and pace control.

Nature communications·2018

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • E2F transcription factors regulate critical cellular processes including apoptosis.
  • E2F1 is a potent inducer of apoptosis, with specific regions dictating this function.
  • Previous research pinpointed the E2F1 marked box and flanking regions as crucial for apoptosis specificity.

Purpose of the Study:

  • To identify proteins interacting with the E2F1 marked box and flanking regions.
  • To investigate the role of these interacting proteins in E2F1-mediated apoptosis.

Main Methods:

  • Yeast two-hybrid screening to identify binding partners of E2F1 regions.
  • Coexpression studies of identified binding partners with E2F1.
  • Analysis of apoptosis induction, p53 protein accumulation, and cell cycle progression.

Related Experiment Videos

  • Gene depletion studies using RNA interference to assess protein function.

    • Main Results:

    • Jab1 was identified as an E2F1-specific binding protein.
    • Coexpression of Jab1 and E2F1 synergistically induced apoptosis and p53 accumulation.
    • Jab1 did not enhance E2F1's role in promoting cell cycle entry.
    • Depletion of Jab1 impaired E2F1-induced apoptosis and p53 induction.

    Conclusions:

    • Jab1 acts as a specific cofactor for E2F1.
    • Jab1 is essential for the apoptotic function of E2F1, likely through p53 pathway modulation.
    • Jab1's role is specific to apoptosis induction and not cell cycle promotion by E2F1.