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

Generation of reversible Rb-knockdown mice.

Yoon Sik Choi1, Jae Eun Lee, Cheolho Cheong

  • 1Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, 300 Chonchon-Dong, Changan-Gu, Suwon 440-746, Republic of Korea.

Mechanisms of Ageing and Development
|August 10, 2005
PubMed
Summary

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

MEGF8 controls osteogenic differentiation through post-transcriptional regulation of BMP-SMAD signaling in craniosynostosis.

Cell death and differentiation·2026
Same author

Species-specific regulation of necroptosis by STK38-dependent RIPK1 phosphorylation.

Cell death and differentiation·2026
Same author

Overcoming Charge-Carrier Localization in Metal Chalcohalides.

Journal of the American Chemical Society·2026
Same author

TRP53/p53 protects adult hippocampal neural stem cells from psychological stress by preventing autophagic cell death.

Autophagy·2026
Same author

Is Photoluminescence Spectroscopy a Suitable Probe of Halide Segregation?

ACS energy letters·2026
Same author

VEGF-B: A multifaceted modulator with emerging therapeutic applications.

Pharmacological research·2025

Researchers created reversible Rb-knockdown mice using a Tet-off system. This method allows conditional control of the Retinoblastoma protein (pRB), offering a new tool for studying gene function in mice.

Area of Science:

  • Molecular Biology
  • Genetics
  • Developmental Biology

Background:

  • The Retinoblastoma protein (pRB) is a crucial tumor suppressor involved in cell cycle regulation.
  • Conventional gene-disrupted mouse models often lack temporal control over gene function.
  • Conditional gene manipulation is essential for studying essential genes and developmental processes.

Purpose of the Study:

  • To develop a Tet-off-inducible system for reversible Retinoblastoma protein (pRB) knockdown in mice.
  • To assess the biological efficacy and reversibility of the generated pRB conditional knockdown system.
  • To evaluate the sufficiency of ectopically expressed pRB in rescuing Rb-/- embryonic phenotypes.

Main Methods:

  • Generation of transgenic mice combining a Tet-off system with a conditional Rb transgene.

Related Experiment Videos

  • Crossing these transgenic mice with conventional Rb+/- mice to create a conditional Rb-/- background.
  • Analysis of cyclin E expression in mouse embryonic fibroblasts (MEFs) to assess doxycycline-dependent pRB regulation.
  • Evaluation of embryonic lethality and phenotypic rescue in Rb-/- embryos.

    • Main Results:

    • Successful generation of mice with Tet-off-controlled, reversible Rb-knockdown.
    • Demonstrated biologically effective and reversible control of transgenic Rb expression, evidenced by doxycycline-dependent cyclin E levels in MEFs.
    • Ectopic pRB expression was insufficient to rescue the organismal-level phenotypes of Rb-/- embryos.
    • Highlighted the need for more complex regulatory mechanisms for pRB function during development.

    Conclusions:

    • The developed Tet-off system provides a viable strategy for creating reversible conditional gene-knockdown mice.
    • This approach offers an alternative to classical gene-disrupted models for studying essential genes like Rb.
    • The findings underscore the intricate regulatory requirements of pRB beyond simple expression levels for proper embryonic development.