Related Experiment Video
Updated: Mar 29, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
Published on: September 28, 2012
Controlling the response to DNA damage by the APC/C-Cdh1
H Rudolf de Boer1, S Guerrero Llobet1, Marcel A T M van Vugt2
1Department of Medical Oncology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
The anaphase-promoting complex/cyclosome (APC/C) with its adaptor protein Cdh1 is activated by DNA damage. This APC/C-Cdh1 complex plays a crucial role in cell cycle regulation and fate determination following DNA damage.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Cell cycle progression relies on cyclin/cyclin-dependent kinase complexes.
- The anaphase-promoting complex/cyclosome (APC/C) is a key regulator of mitotic cyclins.
- APC/C activation by Cdc20 or Cdh1 targets mitotic regulators for degradation, ensuring proper mitosis.
Purpose of the Study:
- To review the regulation of APC/C in response to DNA damage.
- To explore the functions of APC/C-Cdh1 activation upon DNA damage.
- To discuss the role of APC/C-Cdh1 in controlling cell fate with persistent DNA damage.
Main Methods:
- Literature review of in vitro and in vivo studies.
- Analysis of genetic studies on Cdh1-deficient cells.
- Synthesis of current data on APC/C regulation and function.
Main Results:
- APC/C-Cdh1 is activated in G2 phase cells following DNA damage.
- Cdh1 deficiency leads to impaired DNA repair and aberrant cell cycle checkpoints.
- APC/C-Cdh1 activation is a critical response to DNA damage.
Conclusions:
- APC/C-Cdh1 activation is a significant event in the DNA damage response.
- APC/C-Cdh1 influences cell cycle checkpoints and DNA repair.
- Understanding APC/C-Cdh1 function is vital for comprehending cell fate decisions under genotoxic stress.
Related Concept Videos
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Anaphase Promoting Complex
Anaphase Promoting Complex
Inhibition of Cdk Activity
Negative Regulator Molecules

