Jove
Visualize
Contact Us
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 Concept Videos

Overview of DNA Repair02:25

Overview of DNA Repair

30.0K
In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
30.0K
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

3.4K
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...
3.4K
Base Excision Repair01:54

Base Excision Repair

21.9K
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...
21.9K
Duplication of Chromatin Structure02:05

Duplication of Chromatin Structure

5.4K
The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
The basic unit of the chromatin is the nucleosome, consisting of DNA wrapped around octameric histone proteins and short stretches of linker DNA separating individual nucleosomes. The histone proteins within the nucleosome have their...
5.4K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

11.9K
The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
11.9K
Nucleosome Remodeling02:54

Nucleosome Remodeling

8.9K
Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
8.9K

You might also read

Related Articles

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

Sort by
Same author

Polycomb-mediated 3D-genome organization controls replication timing.

Science advances·2026
Same author

Oncolytic adenovirus in combination with PD-L1-targeted radioimmunotherapy exerts synergistic antitumor effect against pancreatic cancer.

Journal for immunotherapy of cancer·2026
Same author

Acid Ceramidase Inhibition Disrupts Ceramide Homeostasis and Induces Mitochondrial Apoptosis in IDH1-Mutant Oligodendroglioma.

Research square·2026
Same author

Clenched fist syndrome: unveiling a motor manifestation of schizophrenia-a case report.

Journal of medical case reports·2026
Same author

Long-term exposure to Di(2-ethylhexyl) phthalate induced uterine histopathologic alterations in female mice.

Toxicology and applied pharmacology·2026
Same author

Alkaline Bromodeoxyuridine (BrdU) Comet Assay to Detect Replication-Associated DNA Damage.

Current protocols·2025
Same journal

Chlorinated VSLSs Surpass HCFCs in CFC-11-Equivalent Emissions for Ozone Layer Depletion in China.

Nature communications·2026
Same journal

Author Correction: Charge transfer in triphenylamine-tetrazine covalent organic frameworks for solar-driven hydrogen peroxide production.

Nature communications·2026
Same journal

Vegetation browning patterns under compound soil and atmospheric dryness in northern permafrost ecosystems.

Nature communications·2026
Same journal

Voltage imaging of CA1 pyramidal cells and SST+ interneurons reveals stability and plasticity mechanisms of spatial firing.

Nature communications·2026
Same journal

Radical-omics reveals the hydrogen-abstraction pathway of isoprene oxidation.

Nature communications·2026
Same journal

Toughening elastomer via sequentially activated multi-pathway energy dissipation.

Nature communications·2026
See all related articles

Related Experiment Video

Updated: May 29, 2025

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.7K

D-2-hydroxyglutarate impairs DNA repair through epigenetic reprogramming.

Fengchao Lang1, Karambir Kaur1, Haiqing Fu2

  • 1Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Nature Communications
|February 7, 2025
PubMed
Summary
This summary is machine-generated.

Isocitrate dehydrogenase (IDH) mutations in cancer cells disrupt DNA repair by altering chromatin structure. The oncometabolite D-2-hydroxyglutarate (D-2-HG) impairs DNA repair protein recruitment, impacting genome stability in IDH-mutant malignancies.

More Related Videos

Steady-state, Pre-steady-state, and Single-turnover Kinetic Measurement for DNA Glycosylase Activity
14:27

Steady-state, Pre-steady-state, and Single-turnover Kinetic Measurement for DNA Glycosylase Activity

Published on: August 19, 2013

19.3K
Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks
12:19

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

8.2K

Related Experiment Videos

Last Updated: May 29, 2025

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

2.7K
Steady-state, Pre-steady-state, and Single-turnover Kinetic Measurement for DNA Glycosylase Activity
14:27

Steady-state, Pre-steady-state, and Single-turnover Kinetic Measurement for DNA Glycosylase Activity

Published on: August 19, 2013

19.3K
Tools to Study the Role of Architectural Protein HMGB1 in the Processing of Helix Distorting, Site-specific DNA Interstrand Crosslinks
12:19

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

8.2K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Mutations in isocitrate dehydrogenase (IDH) are common in various cancers.
  • IDH-mutant cancers display metabolic reprogramming, producing the oncometabolite D-2-hydroxyglutarate (D-2-HG).
  • These cancers exhibit 'BRCAness,' a phenotype characterized by sensitivity to DNA repair inhibitors.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying the DNA repair defects in IDH-mutant cancers.
  • To investigate the role of D-2-HG in chromatin conformation and DNA repair processes.

Main Methods:

  • Analysis of chromatin conformation in IDH-mutant cancer cells.
  • Investigation of D-2-HG's effect on CTCF binding and DNA damage response.
  • Assessment of DNA repair protein (BRCA2, RAD51) recruitment and homologous repair efficiency.

Main Results:

  • D-2-HG disrupts chromatin interactions at DNA damage sites by preventing CTCF binding.
  • D-2-HG-induced hypermethylation suppresses TET1/TET2, leading to CTCF dissociation.
  • CTCF depletion impairs homologous DNA repair by hindering BRCA2 and RAD51 recruitment.

Conclusions:

  • CTCF-mediated chromatin interactions are crucial for efficient DNA damage repair.
  • Oncometabolites like D-2-HG compromise genome stability by disrupting higher-order chromatin structure.
  • Targeting CTCF or related pathways may offer therapeutic strategies for IDH-mutant cancers.