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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...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...

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Related Experiment Video

Updated: Jul 3, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Competition effect in DNA damage response.

Christoph Greubel1, Volker Hable, Guido A Drexler

  • 1LRT2, Universität der Bundeswehr München, 85579 Neubiberg, Germany. christoph.greubel@unibw.de

Radiation and Environmental Biophysics
|July 24, 2008
PubMed
Summary
This summary is machine-generated.

Delayed DNA damage response proteins like 53BP1 and Rad51 accumulate less at later irradiated sites. This suggests a limited protein pool, impacting DNA repair kinetics and potentially radiation therapy outcomes.

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Proximity Ligand Assay to Localize Proteins in DNA Damage Sites
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Last Updated: Jul 3, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Published on: August 21, 2021

Proximity Ligand Assay to Localize Proteins in DNA Damage Sites
09:39

Proximity Ligand Assay to Localize Proteins in DNA Damage Sites

Published on: August 2, 2024

Area of Science:

  • Cell Biology
  • Radiation Biology
  • Molecular Biology

Background:

  • DNA double-strand breaks (DSBs) trigger complex repair pathways.
  • The spatial and temporal dynamics of DSB repair factor accumulation are not fully understood.
  • Understanding DSB repair kinetics is crucial for radiation oncology.

Purpose of the Study:

  • To investigate the impact of sequential, spatially separated DNA damage events on DSB repair.
  • To explore the kinetics of DNA damage response factor accumulation at single-cell level.
  • To assess potential competition for repair factors between distinct damage sites.

Main Methods:

  • Development of an ion-microbeam system for precise, localized irradiation of single cells.
  • Analysis of key DNA damage response proteins (phospho-ATM, gamma-H2AX, Mdc1, 53BP1, Rad51) using immunofluorescence.
  • Quantitative assessment of protein accumulation at early and late microirradiated nuclear sites.

Main Results:

  • Comparable accumulation of early response markers (phospho-ATM, gamma-H2AX, Mdc1) at both early and late irradiation sites.
  • Significant reduction in later response markers (53BP1, Rad51) at late irradiation sites.
  • Evidence of a limited cellular pool of 53BP1, with reduced levels in undamaged areas following irradiation.

Conclusions:

  • The accumulation of DNA repair factors is dependent on the timing and spatial distribution of DNA damage.
  • A limited availability of repair proteins can lead to competition between damage sites, affecting repair efficiency.
  • These findings have implications for optimizing radiation therapy by considering the temporal dynamics of DNA damage response.