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Related Concept Videos

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:
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

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Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.

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The S180R Human Germline Variant of DNA Polymerase β Is a Low Fidelity Enzyme with Reduced Flexibility of the Fingers Domain.

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Protein-Protein Interactions in Base Excision Repair.

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Global screening of base excision repair in nucleosome core particles.

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Collapsed State Mediates the Low Fidelity of the DNA Polymerase β I260 Mutant.

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Related Experiment Video

Updated: May 25, 2026

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

Base excision repair and cancer.

Susan S Wallace1, Drew L Murphy, Joann B Sweasy

  • 1Department of Microbiology and Molecular Genetics, The Markey Center for Molecular Genetics, University of Vermont, Burlington, 05405-0068, United States. susan.wallace@uvm.edu

Cancer Letters
|January 19, 2012
PubMed
Summary

Base excision repair removes daily DNA damage in human cells and is vital for development. Defects in this repair system are linked to cancer and neurological disorders.

Area of Science:

  • Molecular Biology
  • Genetics
  • Human Health

Background:

  • Base excision repair (BER) is a critical DNA repair pathway conserved from bacteria to humans.
  • BER addresses thousands of endogenous DNA damages daily, essential for maintaining genomic integrity.
  • BER dysfunction is implicated in severe health conditions, including cancer and neurological disorders.

Purpose of the Study:

  • To provide an overview of the short-patch base excision repair (SP-BER) pathway in humans.
  • To summarize current research on SP-BER defects in mouse models.
  • To explore the relationship between SP-BER germline polymorphisms and cancer risk.

Main Methods:

  • Review of human SP-BER mechanisms.
  • Analysis of data from mouse models with BER defects.

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence
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Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Related Experiment Videos

Last Updated: May 25, 2026

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

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

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

  • Examination of functional studies on SP-BER germline polymorphisms.
  • Discussion of biallelic germline mutations in MUTYH-associated colon cancer.

    • Main Results:

    • Short-patch base excision repair is crucial for human development.
    • Defects in BER are associated with neurological disorders and cancer.
    • Specific germline polymorphisms in SP-BER may influence cancer susceptibility.
    • MUTYH-associated colon cancer arises from biallelic germline mutations.

    Conclusions:

    • Base excision repair is fundamental for preventing disease.
    • Understanding SP-BER is key to addressing cancer and developmental issues.
    • Further research into SP-BER polymorphisms can illuminate cancer etiology.