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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
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...
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:

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Related Experiment Video

Updated: Jun 10, 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

Tuberous sclerosis complex and DNA repair.

Samy L Habib1

  • 1South Texas Veterans Healthcare System, Geriatric Research, Education and Clinical Center and Department of Medicine, The University of Texas Health Science Center, San Antonio, TX 78229, USA. habib@uthscsa.edu

Advances in Experimental Medicine and Biology
|August 7, 2010
PubMed
Summary

Tuberous sclerosis complex (TSC) is linked to kidney tumors. Loss of TSC2 in Eker rats and human TSC tumors correlates with reduced DNA repair enzyme OGG1 and increased DNA damage, suggesting a role in kidney cancer development.

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Last Updated: Jun 10, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Published on: August 21, 2021

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
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Visualization of DNA Repair Proteins Interaction by Immunofluorescence

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Published on: June 8, 2018

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Tuberous sclerosis complex (TSC) is an autosomal dominant disorder causing hamartomas in multiple organs.
  • TSC is associated with neurological issues and an increased risk of renal cell carcinoma (RCC).
  • Renal angiomyolipomas in TSC patients are often larger, bilateral, and appear earlier than sporadic forms.

Purpose of the Study:

  • To investigate the role of TSC2 and OGG1 in renal tumorigenesis in Tuberous Sclerosis Complex.
  • To explore the relationship between TSC2 deficiency, OGG1 expression, and oxidative DNA damage in kidney tumors.

Main Methods:

  • Utilized heterozygous (TSC2+/-) Eker rats as a model for TSC-associated renal tumors.
  • Analyzed OGG1 expression levels in kidney tissues from Eker rats and human TSC patients with angiomyolipomas.
  • Assessed levels of 8-oxo-deoxyguanine, a marker of oxidative DNA damage, in kidney tumors.

Main Results:

  • Constitutive OGG1 expression was 2-3 fold lower in heterozygous Eker rats and human TSC angiomyolipomas compared to controls.
  • Loss of TSC2 in Eker rat kidney tumors was associated with a concurrent loss of OGG1.
  • Significant accumulation of 8-oxo-deoxyguanine was observed in TSC2-deficient kidney tumors, indicating increased oxidative DNA damage.

Conclusions:

  • TSC2 and OGG1 play a significant role in renal tumorigenesis associated with Tuberous Sclerosis Complex.
  • Reduced OGG1 expression and subsequent DNA damage may contribute to the development of kidney tumors in TSC.
  • Targeting OGG1 or mitigating oxidative stress could be potential therapeutic strategies for TSC-related kidney disease.