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Base Excision Repair

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 Repair

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 Repair

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-pairing and DNA Repair

Base-pairing and DNA Repair

Erwin Chargaff’s rules on DNA equivalence paved the way for the discovery of base pairing in DNA. Chargaff’s rules state that in a double-stranded DNA molecule,

Nucleotide Excision Repair

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 Repair

Nucleotide Excision Repair

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Related Experiment Video

Updated: Jun 16, 2026

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

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

Published on: November 10, 2016

HMGB1: roles in base excision repair and related function.

Yuan Liu¹, Rajendra Prasad, Samuel H Wilson

¹Laboratory of Structural Biology, The National Institute of Environmental Health Sciences, National Institutes of Health, 111 T. W. Alexander Drive Research Triangle Park, NC 27709, USA.

Biochimica Et Biophysica Acta

|February 4, 2010

Summary

High mobility group box 1 (HMGB1) protein regulates DNA repair pathways. It inhibits short DNA repairs while promoting longer ones, impacting genome stability.

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Last Updated: Jun 16, 2026

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

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

Published on: November 10, 2016

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

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Published on: June 26, 2020

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

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

Published on: April 28, 2021

Area of Science:

Molecular Biology
Genetics
Biochemistry

Background:

High mobility group box 1 (HMGB1) is a versatile protein involved in chromatin remodeling, transcription, and inflammation.
Recent findings link HMGB1 to DNA damage repair, specifically the base excision repair (BER) pathway.

Purpose of the Study:

To investigate the specific role of HMGB1 in regulating different sub-pathways of base excision repair.
To understand how HMGB1 influences DNA repair enzyme activity and its implications for genome stability.

Main Methods:

Biochemical assays to analyze HMGB1 interaction with DNA repair intermediates.
Enzyme activity assays to determine HMGB1's modulatory effects on BER enzymes.
Analysis of trinucleotide repeat instability in relation to HMGB1 activity.

Main Results:

HMGB1 acts as a cofactor in the base excision repair pathway.
HMGB1 inhibits single-nucleotide BER while stimulating long-patch BER.
This modulation of BER sub-pathways by HMGB1 is linked to trinucleotide repeat instability.

Conclusions:

HMGB1 plays a critical role in directing DNA repair towards specific sub-pathways.
HMGB1's function in regulating BER contributes to maintaining genome stability.
Targeting HMGB1's role in DNA repair may offer new therapeutic strategies.