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

Cdc6 requires anchorage for its expression.

Shigeki Jinno1, Mika Yageta, Akihisa Nagata

  • 1Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. jinno@m.u-tokyo.ac.jp

Oncogene
|March 16, 2002
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

Gene Expression Profile Signature of Aggressive Waldenström Macroglobulinemia with Chromosome 6q Deletion.

BioMed research international·2018
Same author

Functionalized Fullerene as an Artificial Vector for Transfection.

Angewandte Chemie (International ed. in English)·2018
Same author

General strategy for understanding intracellular molecular interaction cascades that elicit stimulus-invoked biological processes.

Proceedings of the Japan Academy. Series B, Physical and biological sciences·2016
Same author

Gamma Heavy Chain Disease with T-cell Large Granular Lymphocytic Leukemia: A Case Report and Review of the Literature.

Internal medicine (Tokyo, Japan)·2016
Same author

[Achievement of deep molecular response in an elderly chronic myeloid leukemia patient intolerant to imatinib and nilotinib].

[Rinsho ketsueki] The Japanese journal of clinical hematology·2016
Same author

Recombinant human thrombomodulin in the treatment of acute myeloid leukemia patients complicated by disseminated intravascular coagulation: retrospective analysis of outcomes between patients treated with heparin and recombinant human thrombomodulin therapy.

Thrombosis research·2015
Same journal

Aberrant splicing in human cancer shows possible functional impact on transcription factors.

Oncogene·2026
Same journal

The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.

Oncogene·2026
Same journal

Correction: Neuropilin-1 promotes human glioma progression through potentiating the activity of the HGF/SF autocrine pathway.

Oncogene·2026
Same journal

Amphiregulin-mediated EGFR activation drives both intrinsic and acquired resistance to KRAS G12C inhibitors in KRAS G12C-mutant non-small cell lung cancer.

Oncogene·2026
Same journal

Histone lactylation-driven IGF2BP3 promotes intrahepatic cholangiocarcinoma progression via SPP1/CD44-dependent macrophage polarization.

Oncogene·2026
Same journal

Correction: SIRT7 activates p53 by enhancing PCAF-mediated MDM2 degradation to arrest the cell cycle.

Oncogene·2026
See all related articles

Cell anchorage is crucial for fibroblast G1-S phase transition, regulating Cdc6 protein expression. Oncogenic factors override this requirement, enabling anchorage-independent cell cycle progression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Fibroblasts require extracellular matrix anchorage for G1 to S phase transition.
  • Oncogenic transformation alters anchorage dependence in cell cycle regulation.

Purpose of the Study:

  • To investigate the role of Cdc6 protein in anchorage-dependent cell cycle progression.
  • To elucidate the mechanisms by which oncogenic stimulation overrides anchorage requirements.

Main Methods:

  • Analysis of Cdc6 expression in rat fibroblasts upon anchorage loss and oncogenic stimulation.
  • Investigating the role of E2F-dependent promoters and cyclin-dependent kinases (CDKs).

Main Results:

  • Anchorage loss downregulates Cdc6 transcriptionally and post-transcriptionally.

Related Experiment Videos

  • Oncogenic growth factors suppress Cdc6 shutoff and activate Cdk2 and Cdk6/4.
  • Enforced Cdc6 expression bypasses anchorage requirement for G1-S transition.
  • Conclusions:

    • Cdc6 protein requires anchorage or oncogenic stimulation for its function in DNA replication origin activation.
    • G1 cyclin-dependent kinases and Cdc6 are key targets mediating anchorage loss-induced G1-S transition restriction.