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Nucleotide Excision Repair01:08

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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...
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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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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:
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Author Spotlight: Visualizing Single-Stranded DNA During DNA Repair for Therapeutic Insights
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PostExcision Events in Human Nucleotide Excision Repair.

Michael G Kemp1, Jinchuan Hu2

  • 1Department of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, OH.

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|September 21, 2016
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Summary

Nucleotide excision repair removes DNA damage from sunlight. Recent findings show that processing the resulting DNA gaps and fragments is crucial for preventing cell death and diseases like skin cancer.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • The human genome possesses a nucleotide excision repair (NER) system to eliminate diverse DNA lesions, including those from ultraviolet (UV) radiation.
  • NER involves a dual incision mechanism, creating a DNA gap of about 30 nucleotides and releasing a DNA fragment containing the lesion.

Purpose of the Study:

  • To review recent findings on the less-understood post-incision stages of NER.
  • To highlight the significance of processing single-stranded DNA gaps and excised oligonucleotides in the cellular response to DNA damage.

Main Methods:

  • Literature review of recent research on nucleotide excision repair.
  • Analysis of findings related to post-incision gap filling and excised oligonucleotide processing.

Main Results:

  • The fate of single-stranded DNA gaps and excised oligonucleotides in NER has been less studied than initial lesion recognition and incision.
  • Recent studies indicate that the processing of these post-incision intermediates is vital for cellular survival and function.
  • Defects in these later NER stages trigger DNA damage signaling and can lead to cell death.

Conclusions:

  • Post-incision processing of gaps and excised oligonucleotides are critical steps in the cellular response to UV-induced DNA damage.
  • Impairments in these later stages of NER contribute to various human diseases, including skin cancer, aging, and autoimmune disorders.