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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...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
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 6, 2026

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

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Published on: June 9, 2017

Functional interaction between FOXO3a and ATM regulates DNA damage response.

Wen-Bin Tsai1, Young Min Chung, Yoko Takahashi

  • 1Department of Molecular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Nature Cell Biology
|March 18, 2008
PubMed
Summary

FOXO3a directly interacts with ATM, enhancing DNA damage response and repair. This interaction is crucial for activating cell-cycle checkpoints and maintaining genomic stability after DNA breaks.

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Last Updated: Jul 6, 2026

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Genomic stability is vital for preventing mutations and cancer.
  • DNA breaks trigger complex signaling pathways, including the ATM pathway, to initiate repair and cell-cycle arrest.
  • The precise regulation of ATM activation in response to DNA damage is critical.

Purpose of the Study:

  • To investigate the role of FOXO3a in the DNA damage response pathway.
  • To elucidate the interaction between FOXO3a and ATM in DNA repair.
  • To determine how FOXO3a influences ATM-mediated signaling and cell-cycle checkpoints.

Main Methods:

  • Cellular assays to examine protein interactions and phosphorylation.
  • Gene silencing (siRNA) to deplete FOXO3a.
  • Immunofluorescence to detect nuclear foci of ATM and H2AX.
  • Cell-cycle analysis to assess checkpoint activation.

Main Results:

  • FOXO3a interacts with ATM, promoting ATM phosphorylation at Ser 1981 and downstream mediator activation.
  • Silencing FOXO3a prevents the formation of ATM-pS1981 and phospho-histone H2AX foci after DNA damage.
  • Increased FOXO3a enhances ATM signaling, cell-cycle checkpoints (intra-S and G2-M), and DNA repair.
  • FOXO3a's carboxy-terminal domain binds ATM's FAT domain, contributing to ATM activation.

Conclusions:

  • FOXO3a directly regulates ATM activity in the DNA damage response.
  • FOXO3a plays a critical role in activating DNA repair mechanisms and maintaining genomic stability.
  • This interaction highlights a novel regulatory mechanism for ATM in cellular stress response.