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Related Concept Videos

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...
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...
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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...
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...

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Related Experiment Video

Updated: Jul 18, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
10:59

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Fhit modulates the DNA damage checkpoint response.

Hideshi Ishii1, Koshi Mimori, Hiroshi Inoue

  • 1Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.

Cancer Research
|December 6, 2006
PubMed
Summary

The FHIT gene protects cells from DNA damage by regulating checkpoint proteins. Its inactivation contributes to cancer development by causing abnormal checkpoint phenotypes.

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Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The DNA damage checkpoint is activated in preneoplastic lesions.
  • Loss of heterozygosity at the FRA3B/FHIT fragile region is an early event in cancer development.
  • The FHIT gene product (Fhit) plays a role in maintaining genomic stability.

Purpose of the Study:

  • To investigate the role of Fhit in DNA damage checkpoint regulation.
  • To determine the impact of Fhit inactivation on cancer development.
  • To identify key residues in Fhit essential for its function.

Main Methods:

  • Introduction of exogenous Fhit into esophageal cancer cells and noncancerous primary cultures.
  • Analysis of checkpoint protein expression (Hus1 and Chk1) at the mid-S checkpoint.
  • Mutation of the conserved Fhit tyrosine 114 residue to assess its functional importance.

Main Results:

  • Exogenous Fhit modulated expression of checkpoint proteins Hus1 and Chk1, inducing apoptosis in cancer cells but not normal cells.
  • Mutation of Fhit tyrosine 114 abolished its ability to modulate checkpoint proteins and induce apoptosis.
  • Inactivation of Fhit was linked to abnormal checkpoint phenotypes, contributing to cancer progression.

Conclusions:

  • The FRA3B/FHIT fragile region encodes Fhit, a protein crucial for protecting cells against DNA damage accumulation.
  • Fhit functions by modulating checkpoint proteins, and its inactivation is a significant factor in cancer development.
  • Targeting Fhit-mediated pathways may offer therapeutic strategies for esophageal cancer.