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Notably lacking from the biological processes modulated by DNA repair intermediates is that of the protein degradation machinery (e.g. 26S proteasome) which is robustly induced upon exposure to exogenous DNA damaging agents; this suggests that the trigger for upregulating the proteasome emanates from damaged molecules other than DNA, most likely from damaged proteins.
As such, we propose to present the level of mtDNA damage as the percentage of damaged mtDNA in the total DNA content as opposed to the absolute number of damaged molecules.
Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules.
Cytoskeletal functions and polarity are thus crucial for the asymmetrical segregation of damaged molecules.
Second, degraded and damaged molecules that cannot be amplified in the massively parallel amplification step are counted.
However, only in GCV-treated 3MR-expressing senescent cells, we detected smaller (damaged) molecules that migrated faster.
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The signature reaction is strand exchange (mediated by Rad51/RAD51) that occurs between the damaged molecule and an intact donor duplex of homologous sequence.
DOI: http://dx.doi.org/10.7554/eLife.03790.002 Homologous recombination plays an important role in DNA repair in all organisms and acts through the formation of a Holliday junction between the damaged molecule and its repair template.
In nature, these act to neutralise damaging molecules created by ultraviolet light.
In the body, they do the same job – they stabilise damaging molecules on everything from cell membranes to the gut lining and blood vessels.
The resulting cells had impaired energy production, reflected by their high production of oxygen free radicals, damaging molecules generated when energy-generating processes don't run to completion.
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