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Related Concept Videos

CRISPR01:59

CRISPR

Genome editing technologies allow scientists to modify an organism’s DNA via the addition, removal, or rearrangement of genetic material at specific genomic locations. These types of techniques could potentially be used to cure genetic disorders such as hemophilia and sickle cell anemia. One popular and widely used DNA-editing research tool that could lead to safe and effective cures for genetic disorders is the CRISPR-Cas9 system. CRISPR-Cas9 stands for Clustered Regularly Interspaced Short...
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Related Experiment Video

Updated: May 10, 2026

Associated Chromosome Trap for Identifying Long-range DNA Interactions
14:49

Associated Chromosome Trap for Identifying Long-range DNA Interactions

Published on: April 23, 2011

Human CtIP promotes DNA end resection.

Alessandro A Sartori1, Claudia Lukas, Julia Coates

  • 1The Wellcome Trust and Cancer Research UK Gurdon Institute, and Department of Zoology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.

Nature
|October 30, 2007
PubMed
Summary
This summary is machine-generated.

Human CtIP protein is crucial for DNA double-strand break (DSB) repair by promoting DSB resection and homologous recombination. This protein is essential for cell-cycle checkpoint signaling and its function is conserved across species.

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Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
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Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA double-strand breaks (DSBs) trigger cell-cycle checkpoint signaling and repair mechanisms.
  • The MRE11 complex is known to be involved in DSB processing.

Purpose of the Study:

  • To investigate the role of human CtIP (RBBP8) in DNA double-strand break (DSB) repair.
  • To elucidate the relationship between CtIP, the MRE11 complex, and homologous recombination.

Main Methods:

  • Cell cycle analysis of CtIP recruitment to DSBs.
  • Assessment of CtIP's role in DSB resection and RPA/ATR recruitment.
  • Co-immunoprecipitation assays to study CtIP-MRE11 interaction.
  • Homologous recombination assays.
  • Sequence homology analysis with yeast Sae2.

Main Results:

  • CtIP confers resistance to DSB-inducing agents and is recruited to DSBs during S and G2 phases.
  • CtIP is essential for DSB resection, leading to RPA and ATR recruitment and ATR activation.
  • CtIP physically and functionally interacts with the MRE11 complex.
  • Both CtIP and MRE11 are required for efficient homologous recombination.
  • CtIP shows sequence homology to yeast Sae2, suggesting conserved function.

Conclusions:

  • CtIP plays a critical role in DSB resection, checkpoint signaling, and homologous recombination.
  • CtIP functions in concert with the MRE11 complex for efficient DSB repair.
  • CtIP-like proteins have evolutionarily conserved roles in DNA repair pathways.