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Related Concept Videos

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:
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...
Base Excision Repair01:54

Base Excision Repair

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.
The first step of...
Design Consideration01:22

Design Consideration

Designing a structure involves a series of considerations, primarily the material's ultimate strength, calculated through tests that measure changes under increased force until the material reaches its breaking point or limit. The ultimate load, where the material breaks, is divided by its original cross-sectional area, resulting in the ultimate normal stress or strength. The ultimate shearing stress is another significant factor taken into account.
The factor of safety is another key aspect...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview

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Related Experiment Video

Updated: Jun 4, 2026

Induction and Assessment of Exertional Skeletal Muscle Damage in Humans
08:33

Induction and Assessment of Exertional Skeletal Muscle Damage in Humans

Published on: December 11, 2016

A damage limitation exercise.

Andrejs Ivanov, Peter D Adams

    Nature Cell Biology
    |March 3, 2011
    PubMed
    Summary
    This summary is machine-generated.

    Cellular senescence, a tumor suppressor mechanism, involves DNA damage response (DDR) signaling. New findings show that senescence-associated heterochromatin limits DDR, preventing apoptosis and promoting cell survival.

    Area of Science:

    • Cellular and Molecular Biology
    • Cancer Research
    • Epigenetics

    Background:

    • Cellular senescence is a critical tumor suppressor mechanism.

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    Last Updated: Jun 4, 2026

    Induction and Assessment of Exertional Skeletal Muscle Damage in Humans
    08:33

    Induction and Assessment of Exertional Skeletal Muscle Damage in Humans

    Published on: December 11, 2016

    Dosage-Adjusted Resistance Training in Mice with a Reduced Risk of Muscle Damage
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    Dosage-Adjusted Resistance Training in Mice with a Reduced Risk of Muscle Damage

    Published on: August 31, 2022

  • It is characterized by DNA damage response (DDR) signaling and heterochromatinization.
  • The precise role of senescence-associated heterochromatin in regulating DDR and cell fate remains incompletely understood.