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

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

10.4K
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...
10.4K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.4K
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...
3.4K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.6K
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,...
6.6K
Homologous Recombination02:31

Homologous Recombination

65.5K
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...
65.5K
The DNA Replication Fork01:02

The DNA Replication Fork

43.1K
An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
43.1K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

3.2K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K

You might also read

Related Articles

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

Sort by
Same author

Antibody-drug conjugates in selected solid tumours: a position statement update based on findings from the third workshop held by the ETOP IBCSG Partners Foundation.

ESMO open·2026
Same author

Correction: 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 is essential for p53-null cancer cells.

Oncogene·2026
Same author

Black Hole Spectroscopy and Tests of General Relativity with GW250114.

Physical review letters·2026
Same author

High temperature thermal and melting properties of uranium-neptunium and plutonium-neptunium mixed oxides: a MD simulation study.

Physical chemistry chemical physics : PCCP·2026
Same author

GW250114: Testing Hawking's Area Law and the Kerr Nature of Black Holes.

Physical review letters·2025
Same author

Toxicity and efficacy of antibody-drug conjugates in advanced solid tumors: a retrospective single-center analysis of clinical trials.

ESMO open·2025

Related Experiment Video

Updated: Mar 30, 2026

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.5K

RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress.

N Kanu1, T Zhang1, R A Burrell2

  • 1Mammalian Genetics Laboratory, The Francis Crick Institute, London, UK.

Oncogene
|November 10, 2015
PubMed
Summary

Replication stress activates ATM signaling through monoubiquitinated PCNA, a stalled replication fork marker. WRNIP1 bridges this interaction, ensuring genomic stability by activating ATM signaling pathways.

More Related Videos

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.4K
Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

10.7K

Related Experiment Videos

Last Updated: Mar 30, 2026

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

2.5K
Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

11.4K
Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

10.7K

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA replication encounters obstacles, causing replication stress.
  • Replication stress activates ATR and ATM kinases, crucial for DNA repair and genomic stability.
  • The mechanism of ATM activation by replication stress is not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanism of ATM activation in response to replication stress.
  • To identify the key proteins involved in linking stalled replication forks to ATM signaling.

Main Methods:

  • Investigated the interaction between monoubiquitinated PCNA and ATM cofactors.
  • Utilized WRNIP1 and RAD18 in replication stress models.
  • Assessed ATM signaling and 53BP1 focus formation.

Main Results:

  • Monoubiquitinated PCNA interacts with ATM cofactor ATMIN via WRNIP1.
  • ATMIN, WRNIP1, and RAD18 are essential for ATM signaling and 53BP1 focus formation induced by replication stress.
  • This pathway is distinct from ATM activation by ionizing radiation.

Conclusions:

  • WRNIP1 acts as a crucial link between PCNA monoubiquitination and ATMIN/ATM activation.
  • This mechanism is vital for activating ATM signaling during replication stress.
  • The findings contribute to understanding genomic stability maintenance.