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To a certain extent, these damages can be repaired by endogenous DNA repair systems [ 4].
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The majority of single-strand breaks are repaired by endogenous mechanisms in the base excision repair (BER) pathway (65).
While approximately 10000 of these lesions occur daily, most do not go on to harm the cell because they are repaired by endogenous pathways.
The double-strand breaks are repaired by endogenous cellular pathways, including end-joining mechanisms [ e.g., nonhomologous end joining (NHEJ) and theta-mediated end joining (TMEJ)] and homology-dependent repair (HDR) mechanisms (van Schendel et al. 2015).
Most importantly, recent work has shown that developmental defects in FA mice also arise with concomitant inactivation of acetaldehyde metabolism, giving a strong clue about the nature of the endogenous lesion that must be repaired by the functional FA pathway.
The double-strand break is repaired by one of the two endogenous systems, homologous recombination or non-homologous end joining.
Here, we report that the CRISPR/Cas9 system can cleave endogenous gene efficiently in human tripronuclear zygotes, and that the DSBs generated by CRISPR/Cas9 cleavage are repaired by NHEJ and HDR.
Traditionally, these distresses were repaired by partial-depth repair (PDR).
It was repaired by No. 3 Aircraft Depot.
M1dG is repaired by nucleotide excision repair.
Oxidatively damaged DNA is repaired by both base excision repair and nucleotide excision repair [ 7].
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