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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...
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...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview

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Related Experiment Video

Updated: Jun 30, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

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

Published on: September 28, 2012

hCCR4/cNOT6 targets DNA-damage response proteins.

I Sanchez-Perez1, C Manguan-Garcia, M Menacho-Marquez

  • 1Instituto de Investigaciones Biomédicas CSIC/UAM, Dpto. Modelos Experimentales de Enfermedades Humanas, Unidad de Oncologia Translacional. CIBER de Enfermadades Raras Valencia, Spain.

Cancer Letters
|September 27, 2008
PubMed
Summary
This summary is machine-generated.

Researchers identified a new target for cancer therapy by discovering how the hCCR4/CNOT6 gene influences chemotherapy resistance. Targeting this gene may improve treatments for solid tumors.

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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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Related Experiment Videos

Last Updated: Jun 30, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

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

Published on: September 28, 2012

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
05:18

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Published on: June 9, 2020

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

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Chemotherapy is a primary cancer treatment, but drug resistance limits its effectiveness.
  • Understanding resistance mechanisms is crucial for developing novel therapeutic strategies.
  • Genetic suppressor elements (GSEs) offer a method to study gene function in cellular processes.

Purpose of the Study:

  • To identify genes involved in cellular sensitivity or resistance to chemotherapy.
  • To elucidate the role of the identified gene in response to DNA-damaging agents.
  • To explore potential new therapeutic targets for solid tumors.

Main Methods:

  • Selection of genetic suppressor elements (GSEs) conferring resistance to cisplatin.
  • Identification of GSE11 corresponding to the hCCR4/CNOT6 gene.
  • Assessment of hCCR4 protein levels and cellular sensitivity after targeting with GSE11 or siRNA.
  • Analysis of downstream signaling pathways (Chk2, ATM/ATR, histone gammaH2AX phosphorylation) after cisplatin exposure.

Main Results:

  • GSE11, corresponding to the hCCR4/CNOT6 gene, was identified as mediating cellular sensitivity to cisplatin.
  • Reduced hCCR4 protein levels via GSE11 or siRNA decreased mammalian cell sensitivity to DNA-damaging agents.
  • Overexpression of hCCR4 targeted Chk2 post-cisplatin exposure and increased histone gammaH2AX phosphorylation, independent of the ATM/ATR pathway.

Conclusions:

  • The study uncovers a novel function for the human hCCR4 protein in chemotherapy response.
  • Targeting hCCR4 presents a potential new pharmacological strategy for treating solid tumors.
  • This research provides insights into mechanisms of chemotherapy resistance and potential therapeutic interventions.