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Related Concept Videos

Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
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...

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Related Experiment Video

Updated: Jun 30, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

DNA double-strand break rejoining in complex normal tissues.

Claudia E Rübe1, Xiaorong Dong, Martin Kühne

  • 1Department of Radiation Oncology, Saarland University, Homburg/Saar, Saarland, Germany. claudia.ruebe@uks.eu

International Journal of Radiation Oncology, Biology, Physics
|September 23, 2008
PubMed
Summary
This summary is machine-generated.

Tissue radiosensitivity differences are not explained by DNA double-strand break (DSB) repair rates. All normal tissues studied showed identical DSB repair kinetics, indicating other factors influence radiation response.

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Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells
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Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells

Published on: September 8, 2010

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Last Updated: Jun 30, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells
13:10

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells

Published on: September 8, 2010

Area of Science:

  • Radiobiology
  • DNA Damage and Repair
  • Radiation Oncology

Background:

  • Clinical radiation responses vary significantly across different organs.
  • Ionizing radiation induces DNA double-strand breaks (DSBs), a critical determinant of radiosensitivity.
  • The role of DSB repair in normal tissue radiosensitivity is not fully understood.

Purpose of the Study:

  • To investigate if differences in DSB rejoining capacity explain varying clinical radiosensitivity among normal tissues.
  • To quantify DSB induction and repair in complex normal tissues using an in vivo model.

Main Methods:

  • Whole-body irradiation of C57BL/6 mice at doses of 0.1, 0.5, 1.0, and 2.0 Gy.
  • Analysis of DSB formation and rejoining via gammaH2AX foci enumeration in early (small intestine) and late-responding (lung, brain, heart, kidney) tissues.
  • Utilized gammaH2AX immunofluorescence for sensitive DSB detection and quantification.

Main Results:

  • GammaH2AX immunofluorescence accurately quantified DSBs across all analyzed tissues with a linear dose correlation.
  • Identical kinetics for gammaH2AX foci loss were observed in all normal tissues studied.
  • Despite identical DSB repair kinetics, tissues exhibited distinct clinical radiation responses.

Conclusions:

  • Tissue-specific differences in radiation response are independent of DSB rejoining capacity.
  • DSB repair plays a fundamental role in maintaining genomic integrity, cellular viability, and tissue homeostasis.
  • Findings suggest other mechanisms contribute to differential radiosensitivity among normal tissues.