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Related Experiment Video

Updated: May 4, 2026

Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks
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Triplex-induced DNA damage response.

Faye A Rogers1, Meetu Kaushik Tiwari1

  • 1Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.

The Yale Journal of Biology and Medicine
|December 19, 2013
PubMed
Summary

The DNA damage response pathway, involving the TFIIH factor XPD, triggers apoptosis to maintain genomic integrity against structural DNA damage like triplexes.

Keywords:
DNA repairH-DNAH2AXXPDapoptosisgenomic instabilitynucleotide excision repairtriplex DNAtriplex-forming oligonucleotides

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Cellular DNA damage response is crucial for genomic integrity.
  • Complex signaling pathways manage DNA damage, leading to cell cycle arrest, repair, or apoptosis.
  • Altered DNA helical structures, such as triplexes, present unique genotoxic stress.

Purpose of the Study:

  • To investigate cellular pathways processing DNA damage induced by triplex structures.
  • To elucidate the role of TFIIH factor XPD in apoptosis following triplex-induced DNA damage.

Main Methods:

  • Investigated co-localization of XPD with γH2AX.
  • Assessed the requirement of XPD for H2AX phosphorylation at tyrosine 142.
  • Examined cellular pathways activated by triplex formation.

Main Results:

  • TFIIH factor XPD plays a key role in initiating apoptosis in response to triplex-induced DNA strand breaks.
  • XPD co-localizes with γH2AX at DNA damage sites.
  • XPD is essential for H2AX tyrosine 142 phosphorylation, recruiting pro-apoptotic factors.

Conclusions:

  • XPD-dependent apoptosis is a critical mechanism for preserving genomic integrity when faced with excessive structurally induced DNA damage.
  • Understanding these pathways can inform strategies for managing genotoxic stress.