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Nucleotide Excision Repair01:38

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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...
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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DNA Oxidation and Excision Repair Pathways.

Tae-Hee Lee1, Tae-Hong Kang1

  • 1Department of Biological Science, Dong-A University, Busan 49315, Korea.

International Journal of Molecular Sciences
|December 11, 2019
PubMed
Summary
This summary is machine-generated.

Genomic DNA repair is crucial. The nucleotide excision repair (NER) pathway collaborates with base excision repair (BER) to mitigate oxidative DNA damage, preventing cancer and neurological issues.

Keywords:
base excision repair (BER)nucleotide excision repair (NER)oxidative DNA damagereactive oxygen species (ROS)

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Genomic DNA is constantly under assault from oxidative damage.
  • The base excision repair (BER) pathway is the primary defense against non-bulky DNA oxidation.
  • Impairment in BER leads to embryonic lethality, cancer susceptibility, and neurological symptoms.

Purpose of the Study:

  • To explore the involvement of other DNA repair pathways in mitigating oxidative DNA damage.
  • To investigate the roles of nucleotide excision repair (NER) factors in DNA repair.
  • To understand the interplay between BER and NER pathways in response to genotoxic oxidative stress.

Main Methods:

  • Review of recent scientific literature on DNA repair mechanisms.
  • Analysis of studies investigating the roles of NER lesion recognition factors.
  • Examination of cooperative functions between BER and NER pathways.

Main Results:

  • NER pathway factors play significant roles in recognizing DNA oxidation lesions.
  • NER factors can stimulate the activity of certain BER pathway components.
  • Substantial bulky DNA oxidation can be repaired by the canonical NER mechanism.

Conclusions:

  • NER pathway factors have newly identified roles in facilitating the BER process.
  • Cooperative action between BER and NER pathways is essential for managing genotoxic oxidative stress.
  • Dysfunction in NER, like BER, can lead to cancer predisposition and neurological disorders.