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[70] γH2AX (H2AX phosphorylated on serine 139) can be detected as soon as 20 seconds after irradiation of cells (with DNA double-strand break formation), and half maximum accumulation of γH2AX occurs in one minute. [70] The extent of chromatin with phosphorylated γH2AX is about two million base pairs at the site of a DNA double-strand break.
Further work by Allen et al. [150] showed that NHEJ of a DNA double-strand break in a cell could give rise to some progeny cells having repressed expression of the gene harboring the initial double-strand break and some progeny having high expression of that gene due to epigenetic alterations associated with NHEJ repair. The frequency of ...
A double-strand break repair model refers to the various models of pathways that cells undertake to repair double strand-breaks (DSB). DSB repair is an important cellular process, as the accumulation of unrepaired DSB could lead to chromosomal rearrangements, tumorigenesis or even cell death. [ 1 ]
The RecBCD pathway is the main recombination pathway used in many bacteria to repair double-strand breaks in DNA, and the proteins are found in a broad array of bacteria. [63] [64] [65] These double-strand breaks can be caused by UV light and other radiation, as well as chemical mutagens.
Single-strand breaks (SSBs) occur when one strand of the DNA double helix experiences breakage of a single nucleotide accompanied by damaged 5’- and/or 3’-termini at this point. One common source of SSBs is due to oxidative attack by physiological reactive oxygen species (ROS) such as hydrogen peroxide.
The production of ROS in high quantity in cells results in the degradation of biomolecules such as proteins, DNA, and RNA. In one such instance the ROS are known to create double stranded and single stranded breaks in the DNA. This causes the DNA repair mechanisms to try to adapt to the increase in DNA strand breaks.
Normal replication stress occurs at low to mild levels and induces genomic instability, which can lead to tumorigenesis and cancer progression. [18] However, high levels of replication stress have been shown to kill cancer cells. In one study, researchers sought to determine the effects of inducing high levels of replication stress on cancer cells.
Some chromosomes have fragile spots where breaks occur, which result in the deletion of a part of the chromosome. The breaks can be induced by heat, viruses, radiation, or chemical reactions. When a chromosome breaks, if a part of it is deleted or lost, the missing piece of chromosome is referred to as a deletion or a deficiency. [2]