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

Cell cycle attenuation by p120E4F is accompanied by increased mitotic dysfunction.

R J Rooney1

  • 1Department of Genetics, Duke University Medical Center, Durham, North Carolina 27710, USA. robert.rooney@duke.edu

Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|October 30, 2001
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

Expression of GABAA α2-, β1- and ε-receptors are altered significantly in the lateral cerebellum of subjects with schizophrenia, major depression and bipolar disorder.

Translational psychiatry·2013
Same author

mRNA and protein expression for novel GABAA receptors θ and ρ2 are altered in schizophrenia and mood disorders; relevance to FMRP-mGluR5 signaling pathway.

Translational psychiatry·2013
Same author

Examination of the antibacterial properties of sphagnum moss (Sphagnum spp.) and its significance with turf burning in Ireland.

British journal of biomedical science·2013
Same author

Mining the antibiogram: what more can it tell us?

British journal of biomedical science·2012
Same author

Distinct gene signature revealed in white blood cells, CD4(+) and CD8(+) T cells in (NZBx NZW) F1 lupus mice after tolerization with anti-DNA Ig peptide.

Genes and immunity·2010
Same author

Should long-haul flights carry antibiotics on board to treat acute bacterial meningitis and meningococcal septicaemia?

British journal of biomedical science·2009

Elevated cyclin-dependent kinase (CDK) inhibitors can disrupt G2-M cell cycle progression and cytokinesis, leading to polyploidy. This study shows moderate CDK inhibitor increases impede G2-M function and may initiate endomitosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Cyclin-dependent kinase (CDK) inhibitors are known regulators of the G1-S checkpoint.
  • Emerging evidence suggests universal CDK inhibitors also play a role in G2-M checkpoint control.
  • Their induction may contribute to endomitosis and polyploidy in various physiological contexts.

Purpose of the Study:

  • To investigate the role of the p120E4F transcription factor in cell cycle regulation beyond G1-S.
  • To determine the impact of p120E4F expression on G2-M progression and cytokinesis.
  • To explore the relationship between CDK inhibitors, cell cycle progression, and polyploidy.

Main Methods:

  • Stable expression of the p120E4F transcription factor in fibroblast cell lines.

Related Experiment Videos

  • Analysis of CDC2 kinase activity and Cyclin B1 protein levels.
  • Assessment of cell ploidy and multinucleation.
  • Coexpression of activated Ras to modulate G1-S specific cyclin-CDK activities.

    • Main Results:

    • p120E4F expression reduced CDC2 kinase activity and elevated Cyclin B1 protein levels.
    • Fibroblast cell lines expressing p120E4F showed increased tetraploid and multinucleated cells.
    • Coexpression with Ras alleviated these effects, restoring CDC2-Cyclin B activity and reducing polyploidy.
    • Changes in Cyclin B1 and CDC2 levels were mainly post-transcriptional.

    Conclusions:

    • Moderate elevation of CDK inhibitors can impair G2-M function by reducing CDC2 kinase activity.
    • Sustained CDK2 kinase activity and elevated CDK inhibitors may be sufficient to induce endomitosis.
    • The findings highlight a potential mechanism for polyploidy development in physiological settings.