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Related Concept Videos

S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...

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Related Experiment Video

Updated: May 10, 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

Controlling DNA-end resection: a new task for CDKs.

Lorenza P Ferretti1, Lorenzo Lafranchi, Alessandro A Sartori

  • 1Institute of Molecular Cancer Research, Faculty of Medicine, University of Zurich Zurich, Switzerland.

Frontiers in Genetics
|June 14, 2013
PubMed
Summary

Cyclin-dependent kinases (CDKs) regulate DNA double-strand break (DSB) repair by controlling DNA-end resection. This phosphorylation mechanism ensures accurate repair, preventing genomic instability and tumorigenesis.

Keywords:
CtIP/Sae2DNA double-strand break repairDNA-end resectionPIN1cyclin-dependent kinasehomologous recombinationphosphorylation

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence

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Related Experiment Videos

Last Updated: May 10, 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

Visualizing Single-Stranded DNA Foci in the G1 Phase of the Cell Cycle
08:30

Visualizing Single-Stranded DNA Foci in the G1 Phase of the Cell Cycle

Published on: December 22, 2023

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA double-strand breaks (DSBs) are critical DNA lesions repaired by homologous recombination (HR) and non-homologous end-joining (NHEJ).
  • The cell cycle tightly regulates the choice between HR and NHEJ pathways.
  • DNA-end resection is a key process that favors HR and suppresses NHEJ.

Purpose of the Study:

  • To review the regulatory role of cyclin-dependent kinases (CDKs) in DNA-end resection.
  • To highlight the importance of CDK-mediated phosphorylation in controlling DSB repair pathway choice.
  • To summarize current understanding of CDK regulation of resection machinery in yeast and human cells.

Main Methods:

  • Literature review of recent research on DNA repair mechanisms.
  • Focus on post-translational modifications, specifically phosphorylation at S/T-P motifs.
  • Analysis of CDK substrates involved in DNA-end resection.

Main Results:

  • CDK activity is crucial for the timely and coordinated execution of DNA-end resection.
  • Key DNA-end resection factors are identified as CDK substrates.
  • Phosphorylation by CDKs represents a major regulatory mechanism for DSB repair pathway choice.

Conclusions:

  • CDK-mediated phosphorylation is a critical regulator of DNA-end resection.
  • Understanding this regulation is vital for comprehending genomic stability and preventing cancer.
  • This mechanism ensures accurate DSB repair by directing the appropriate pathway choice.