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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...
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

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Nucleotide Excision Repair01:08

Nucleotide Excision Repair

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Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

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Updated: Jun 12, 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

Mi-2/NuRD complex making inroads into DNA-damage response pathway.

Da-Qiang Li1, Rakesh Kumar

  • 1Department of Biochemistry and Molecular Biology, George Washington University Medical Center, Washington, DC, USA.

Cell Cycle (Georgetown, Tex.)
|May 28, 2010
PubMed
Summary
This summary is machine-generated.

The Mi-2/nucleosome remodeling and histone deacetylation (NuRD) complex, particularly its component MTA1, is newly linked to DNA damage response pathways. This review explores its role in DNA repair, alongside histone modifications and chromatin remodeling.

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Published on: June 9, 2017

Area of Science:

  • Cellular biology
  • Molecular genetics
  • Epigenetics

Background:

  • Eukaryotic DNA is packaged into chromatin, a condensed structure that can impede DNA access for cellular processes.
  • Histone modifications and ATP-dependent chromatin remodeling are key mechanisms cells use to regulate chromatin structure and facilitate DNA accessibility.
  • While known for transcriptional regulation, these mechanisms are also crucial for DNA repair.

Purpose of the Study:

  • To review the established roles of histone modifications and chromatin remodeling in DNA repair.
  • To highlight the emerging role of the Mi-2/nucleosome remodeling and histone deacetylation (NuRD) complex in DNA damage response.
  • To connect the functions of the Mi-2/NuRD complex with DNA repair research.

Main Methods:

  • Literature review focusing on DNA repair, histone modifications, and chromatin remodeling.
  • Analysis of recent findings on the Mi-2/NuRD complex and its components, such as MTA1, in DNA damage pathways.
  • Synthesis of information linking chromatin regulation to DNA repair mechanisms.

Main Results:

  • Histone modifications and ATP-dependent chromatin remodelers are vital for efficient DNA repair.
  • The Mi-2/NuRD complex, possessing both remodeling and deacetylase activities, has a significant, previously underappreciated role in DNA damage response.
  • Metastasis-associated protein 1 (MTA1), a component of Mi-2/NuRD, is a key player linking this complex to DNA repair pathways.

Conclusions:

  • The Mi-2/NuRD complex represents a critical link between chromatin regulation and DNA damage response.
  • Further research into the Mi-2/NuRD complex's function in DNA repair is warranted.
  • Understanding these mechanisms can provide insights into cellular resilience and disease.