Jove
Visualize
Contact Us

Related Concept Videos

Base Excision Repair01:54

Base Excision Repair

27.6K
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...
27.6K
Base Excision Repair01:54

Base Excision Repair

5.5K
5.5K
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

8.2K
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:
8.2K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

5.6K
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...
5.6K
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

41.9K
Overview
41.9K
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

13.9K
13.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Radiosensitisation of Head and Neck Cancer Cells to Protons of Increasing LET Through Targeting DNA Double Strand Break Repair.

Cells·2026
Same author

Understanding and Exacerbating the Biological Response of Uveal Melanoma to Proton Beam Therapy.

Cancers·2025
Same author

Adverse drug reaction profiles of histone deacetylase inhibitors.

Scientific reports·2025
Same author

Assessing the Relative Contribution of DSB Repair Proteins as a Function of LET.

International journal of particle therapy·2025
Same author

Radiobiological characterisation of a 28 MeV proton beam delivered by the MC-40 cyclotron.

Cell death discovery·2025
Same author

Targeting Chk1 and Wee1 kinases enhances radiosensitivity of 2D and 3D head and neck cancer models to X-rays and low/high-LET protons.

Cell death & disease·2025
Same journal

ZRANB1 and ACSS2 Cooperate to Regulate Ubiquitination and Acetylation to Stabilize TWIST1 in Breast Cancer Metastasis.

Molecular and cellular biology·2026
Same journal

Gasdermin D Inhibition Attenuates Mitochondrial Damage and Cardiomyocyte Pyroptosis in Heart Failure with Preserved Ejection Fraction.

Molecular and cellular biology·2026
Same journal

Dual Sub‑MIC Copper-Gentamicin Stress Drives Strain‑Specific, Non‑Additive Phenotypic Shifts in <i>Pseudomonas aeruginosa</i>.

Molecular and cellular biology·2026
Same journal

Transcription Factors in Breast Cancer Oncogenesis and Progression.

Molecular and cellular biology·2026
Same journal

Aberrant Expression of miR-25-3p/EZH2 Is Involved in T Cell Activation in Aplastic Anemia.

Molecular and cellular biology·2026
Same journal

Characterization of the m<sup>6</sup>A Epitranscriptome in Fibroblast Senescence.

Molecular and cellular biology·2026
See all related articles
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: Mar 24, 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

4.7K

Base Excision Repair, a Pathway Regulated by Posttranslational Modifications.

Rachel J Carter1, Jason L Parsons2

  • 1North West Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.

Molecular and Cellular Biology
|March 16, 2016
PubMed
Summary
This summary is machine-generated.

Post-translational modifications (PTMs) regulate base excision repair (BER) proteins, influencing DNA repair efficiency and genome stability. Understanding these PTMs is crucial for preventing diseases like cancer.

More Related Videos

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

4.2K
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.3K

Related Experiment Videos

Last Updated: Mar 24, 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

4.7K
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

4.2K
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.3K

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Base excision repair (BER) is a critical DNA repair pathway for maintaining genome stability.
  • Dysregulation of BER is implicated in human diseases, including cancer, neurodegenerative disorders, and premature aging syndromes.
  • Protein post-translational modifications (PTMs) are increasingly recognized as key regulators of cellular processes.

Purpose of the Study:

  • To review the current knowledge on post-translational modifications (PTMs) of key base excision repair (BER) proteins.
  • To elucidate the functional consequences of these PTMs on BER protein activity, interactions, and localization.
  • To discuss the impact of PTMs on the overall efficiency of the BER pathway in vitro and in vivo.

Main Methods:

  • Literature review of studies characterizing PTMs in BER proteins.
  • Analysis of functional data related to PTMs' impact on protein level and activity.
  • Synthesis of in vitro and in vivo experimental findings on PTMs in BER.

Main Results:

  • Several PTMs, including acetylation, methylation, phosphorylation, SUMOylation, and ubiquitylation, have been identified in key BER proteins.
  • These modifications modulate BER protein levels, enzymatic activities, protein-protein interactions, and cellular localization.
  • PTMs play a significant role in fine-tuning the BER pathway's response to DNA damage.

Conclusions:

  • Post-translational modifications are crucial regulators of the base excision repair pathway.
  • Understanding PTMs of BER proteins is essential for comprehending genome stability maintenance and disease prevention.
  • This review consolidates current data, highlighting PTMs as critical targets for future research in DNA repair and disease.