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Related Concept Videos

Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

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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...
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Homologous Recombination02:31

Homologous Recombination

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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...
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Overview of DNA Repair02:25

Overview of DNA Repair

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Overview of DNA Repair02:25

Overview of DNA Repair

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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.
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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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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Related Experiment Video

Updated: May 2, 2026

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
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Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

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DNA double-strand break repair in a cellular context.

A Shibata1, P A Jeggo2

  • 1Advanced Scientific Research Leaders Development Unit, Gunma University, Maebashi, Gunma, Japan.

Clinical Oncology (Royal College of Radiologists (Great Britain))
|March 18, 2014
PubMed
Summary

This study reviews DNA double-strand break repair pathways and their cell cycle interactions. Understanding these mechanisms in cancer cells can reveal new therapeutic targets.

Keywords:
DNA damage response signallingDNA non-homologous end-joiningDSB repairhomologous recombinationradiationradiotherapy

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Last Updated: May 2, 2026

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
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Area of Science:

  • Molecular biology
  • Biochemistry
  • Structural biology

Background:

  • DNA double-strand breaks (DSBs) are critical DNA lesions.
  • Existing research provides molecular, biochemical, and structural insights into DSB repair.
  • Focus is shifting towards understanding pathway interplay and cell cycle integration.

Purpose of the Study:

  • To overview DSB repair processes.
  • To discuss the interplay between DSB repair pathways.
  • To explore the connection between DSB repair, cell cycle, replication, and transcription.

Main Methods:

  • Molecular approaches
  • Biochemical assays
  • Structural biology techniques

Main Results:

  • DSB repair involves complex, interconnected pathways.
  • These pathways interface with the cell cycle, replication, and transcription.
  • Cancer cells may exploit these processes for proliferation.

Conclusions:

  • Understanding DSB repair interplay is crucial for cancer biology.
  • Identifying therapeutic targets for cancer treatment is a key outcome.