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Related Concept Videos

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
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
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:
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...

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Related Experiment Video

Updated: Jul 4, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Tissue-specific accelerated aging in nucleotide excision repair deficiency.

Laura J Niedernhofer1

  • 1Department of Microbiology and Molecular Genetics, UP Cancer Institute, University of Pittsburgh School of Medicine, 5117 Centre Avenue, Pittsburgh, PA 15213, USA. niedernhoferl@upmc.edu

Mechanisms of Ageing and Development
|June 10, 2008
PubMed
Summary

Nucleotide excision repair (NER) removes DNA damage to prevent mutations and cell death. Defects in NER lead to premature aging syndromes like xeroderma pigmentosum, highlighting DNA repair

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Nucleotide excision repair (NER) is a critical DNA repair pathway.
  • NER removes helix-distorting DNA lesions.
  • NER comprises two subpathways: global genome NER and transcription-coupled (TC)-NER.

Purpose of the Study:

  • To review the mechanisms of NER.
  • To discuss the link between DNA damage, NER, and premature aging.
  • To emphasize accelerated aging in xeroderma pigmentosum.

Main Methods:

  • Literature review of DNA repair mechanisms.
  • Analysis of genetic defects in NER.
  • Examination of clinical manifestations of NER deficiency syndromes.

Main Results:

  • NER prevents mutation accumulation and cell death from DNA damage.
  • Defects in NER cause xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy.
  • These syndromes exhibit premature aging phenotypes affecting multiple tissues.

Conclusions:

  • DNA damage significantly contributes to age-related diseases.
  • NER failure underlies premature aging and associated pathologies.
  • Understanding NER is crucial for addressing age-related conditions and DNA repair disorders.