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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

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Related Experiment Video

Updated: Jun 21, 2026

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry
08:21

Cell Cycle-specific Measurement of γH2AX and Apoptosis After Genotoxic Stress by Flow Cytometry

Published on: September 1, 2019

Modeling radiation-induced cell cycle delays.

Anna Ochab-Marcinek1, Ewa Gudowska-Nowak, Elena Nasonova

  • 1Department of Soft Condensed Matter, Institute of Physical Chemistry, Polish Academy of Sciences, ul. Kasprzaka 44/52, Warsaw, Poland. ochab@ifka.ichf.edu.pl

Radiation and Environmental Biophysics
|August 12, 2009
PubMed
Summary

This study introduces a new method to track cell cycle changes after radiation exposure using only mitotic index data. It reveals a G2 phase block in damaged cells, crucial for understanding radiation effects and risks.

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One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
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One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy

Published on: October 23, 2017

Area of Science:

  • Cell biology
  • Radiation biology
  • Genetics

Background:

  • Ionizing radiation is known to disrupt cell cycle progression.
  • Cell cycle delays influence damage expression, like chromosome aberrations.
  • Accurate radiation risk assessment requires understanding radiation-induced cell cycle perturbations.

Purpose of the Study:

  • To develop and apply a method for retrieving cell cycle phase dynamics from mitotic index data.
  • To analyze mammalian cell cycle progression following radiation exposure.
  • To provide insights into radiation-induced cell cycle delays.

Main Methods:

  • Utilized experimental data on the mitotic index.
  • Developed a method to infer the time-course of all cell cycle phases.
  • Performed error analysis on simulated data to guide experimental design.

Main Results:

  • Identified a prolonged G2 phase block in damaged cells after exposure.
  • Demonstrated the feasibility of reconstructing cell cycle kinetics from mitotic index data.
  • Determined that analyzing at least 100 cells per sample is necessary for <20% relative error.

Conclusions:

  • The developed method allows for detailed cell cycle analysis post-irradiation using limited data.
  • The findings highlight the G2 phase as a critical checkpoint for radiation-damaged cells.
  • This approach aids in optimizing experimental design for radiation biology studies.