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Related Concept Videos

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...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:

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Updated: Jun 27, 2026

Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair
10:59

Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair

Published on: May 24, 2017

UV-DDB as a Dynamic Regulator Linking Base Excision and Nucleotide Excision Repair via AAG Interaction.

Jiwon Eom1,2, Yubin Ko1,2, Jeongwoo Choi1,2

  • 1Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul 03760, Republic of Korea.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary

The ultraviolet (UV)-damaged DNA-binding protein (UV-DDB) directly interacts with alkyladenine DNA glycosylase (AAG). DNA binding reconfigures this interaction, suggesting UV-DDB recruits AAG for base excision repair (BER) pathway progression.

Keywords:
AlphaFold3UV-damaged DNA-binding protein (UV-DDB)alkyladenine DNA glycosylase (AAG)base excision repair (BER)biolayer interferometry (BLI)nucleotide excision repair (NER)surface plasmon resonance (SPR)

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Area of Science:

  • Molecular Biology
  • DNA Repair Mechanisms
  • Structural Biology

Background:

  • Base excision repair (BER) and nucleotide excision repair (NER) are distinct DNA repair pathways.
  • Ultraviolet (UV)-damaged DNA-binding protein (UV-DDB), a key NER factor, is known to stimulate BER DNA glycosylases like alkyladenine DNA glycosylase (AAG).
  • The precise molecular basis and DNA-mediated regulation of the UV-DDB/AAG interaction remain largely uncharacterized.

Purpose of the Study:

  • To investigate the direct physical interaction between AAG and UV-DDB.
  • To elucidate how DNA binding influences the UV-DDB/AAG complex formation and structure.
  • To provide a structural framework for the coordinated action of BER and NER pathways.

Main Methods:

  • Electrophoretic mobility shift assays (EMSA) were used to assess complex formation.
  • Surface plasmon resonance (SPR) and biolayer interferometry (BLI) quantified interaction affinities under DNA-free and DNA-bound conditions.
  • AlphaFold3-based structural modeling predicted the atomic details of the UV-DDB/AAG complex with and without DNA.

Main Results:

  • SPR and BLI confirmed a high-affinity direct interaction between AAG and UV-DDB, with affinity modulated by the presence of apurinic/apyrimidinic (AP) site-containing DNA.
  • EMSA demonstrated UV-DDB's role in forming ternary complexes and influencing AAG/DNA binary species distribution.
  • AlphaFold3 modeling revealed distinct AAG binding modes: to DDB1 in the DNA-free state and repositioning towards the DNA lesion via DDB2 upon DNA binding.

Conclusions:

  • DNA binding acts as a molecular switch, reconfiguring the UV-DDB/AAG interaction.
  • This reconfiguration facilitates UV-DDB's function as a platform for recruiting AAG, promoting efficient base excision repair.
  • The study provides structural insights into the coordinated integration of BER and NER pathways.