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

Homologous Recombination02:31

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Conservative Site-specific Recombination and Phase Variation02:53

Conservative Site-specific Recombination and Phase Variation

Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
The recognition sites for Cre recombinase called LoxP...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

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...

You might also read

Related Articles

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

Sort by
Same author

Impact of <i>N</i>-Acetylation on DNA Damage and Oxidative Stress Responses in Mammalian Cells and Human Hepatocytes Treated with Hydralazine.

Biomolecules·2026
Same author

A Survey of DNA Damage in American Alligators (Alligator mississippiensis) in Florida.

Environmental and molecular mutagenesis·2026
Same author

Hexavalent Chromium Oropharyngeal Aspiration Induced Behavior Effects and Essential Metal Dyshomeostasis in Young Hartley Guinea Pigs.

Applied sciences (Basel, Switzerland)·2026
Same author

It's a gator tale: Alligator lung cells resist hexavalent chromium-induced DNA repair inhibition and chromosome instability.

Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)·2026
Same author

Arylamine N-Acetyltransferase 1 Knockout in Immortalized Human Bronchial Cells Results in a Reduction of Cellular Growth.

Gene reports·2025
Same author

Brevetoxin Dynamics and Bioavailability from Floc Following PAC-Modified Clay Treatment of <i>Karenia brevis</i> Blooms.

Toxins·2025
Same journal

Medcical services at work.

Occupational Health·1972
Same journal

Industrial chaplaincy.

Occupational Health·1972
Same journal

The incidence of industrial eye injuries in New Zealand & their causes.

Occupational Health·1972
Same journal

The role & functions of an occupational health clinic.

Occupational Health·1972
Same journal

Industrial injuries: an orthopaedic view.

Occupational Health·1972
Same journal

The damaged eye.

Occupational Health·1971
See all related articles

Related Experiment Video

Updated: May 23, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
06:24

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Particulate Hexavalent Chromium Inhibits RAD51 Paralogs Necessary for RAD51 Filament Formation and Stabilization

Aggie R Williams1, Idoia Meaza1, Haiyan Lu1

  • 1Wise Laboratory of Environmental and Genetic Toxicology, Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40202, USA.

Occupational Health
|May 22, 2026
PubMed
Summary
This summary is machine-generated.

Hexavalent chromium (Cr(VI)) exposure represses RAD51 paralogs, crucial for DNA repair. Cr(VI) impairs homologous recombination repair by targeting RAD51D early, hindering DNA repair and potentially causing lung cancer.

Keywords:
DNA repair inhibitionRAD51 paralogshexavalent chromiumlung cancermechanisms of carcinogenesismetal exposure

More Related Videos

Preparation of the Mgm101 Recombination Protein by MBP-based Tagging Strategy
11:40

Preparation of the Mgm101 Recombination Protein by MBP-based Tagging Strategy

Published on: June 25, 2013

Related Experiment Videos

Last Updated: May 23, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
06:24

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

Preparation of the Mgm101 Recombination Protein by MBP-based Tagging Strategy
11:40

Preparation of the Mgm101 Recombination Protein by MBP-based Tagging Strategy

Published on: June 25, 2013

Area of Science:

  • Molecular Biology
  • Environmental Health
  • Genetics

Background:

  • Hexavalent chromium (Cr(VI)) is a known lung carcinogen.
  • Cr(VI) induces DNA double-strand breaks and chromosome instability.
  • Cr(VI) impairs homologous recombination repair by targeting RAD51.

Purpose of the Study:

  • To investigate the effects of Cr(VI) exposure on RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, XRCC3).
  • To understand the role of RAD51 paralogs in Cr(VI)-induced DNA damage and repair inhibition.

Main Methods:

  • Exposure of WTHBF-6 human lung cells to zinc chromate.
  • RNA sequencing, RT-qPCR, Western blotting, and immunofluorescence assays.
  • Proximity Ligation Assay (PLA) to assess protein-protein interactions.

Main Results:

  • Cr(VI) exposure transcriptionally repressed all RAD51 paralogs.
  • Cr(VI) inhibited RAD51D foci formation after acute and prolonged exposure.
  • Cr(VI) inhibited XRCC2 and XRCC3 foci formation after prolonged exposure.
  • Cr(VI) reduced RAD51D protein levels and its interaction with RAD51.

Conclusions:

  • Cr(VI) inhibits all RAD51 paralogs, suggesting a broad impact on homologous recombination repair.
  • RAD51D may be an early target of Cr(VI), leading to impaired RAD51 filament formation and function.
  • Cr(VI) significantly disrupts DNA repair mechanisms, contributing to its carcinogenic potential.