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However, in most cases, the proteins targeted by these deleterious modifications as well as their consequences have not yet been clearly identified.
It has been found that free radical reactions can produce deleterious modifications in membranes, proteins, enzymes, and DNA [2], increasing the risk of diseases such as cancer [3], Alzheimer's [4], Parkinson's [5], angiocardiopathy [6], arthritis [7], asthma [8], diabetes [9], and degenerative eye disease [10].
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It is striking to observe that this deleterious modification is widely found in available IRES-containing vectors, including commercial ones, despite early reports in the literature stating the importance of the integrity of the initiation codon for optimal IRES function.
For example, beneficial effects of novel food may outweigh deleterious habitat modifications.
GSH had an essential role in preserving nuclear function from deleterious oxidative modifications.
Therefore, in addition to the possibility identified by Olson's theory, in which loss of function is driven by environmental changes, synthetic rescues indicate that loss of gene function may also be driven by a previous deleterious genetic modification.
Modification of conserved C156 resulted in a two-fold reduction in expression level but not a significant change in solubility until combined with a non-deleterious Q181R modification.
By virtue of its interaction with the N17 domain, TRiC might provide a protective effect against deleterious post-translational modifications.
Having ruled out mitochondrial biogenesis as a potential mechanism underlying the effects of EPA on mitochondrial function, we discovered that EPA reduced deleterious post-translational modifications, most notably carbamylation of mitochondrial proteins.
Surprisingly, while single nucleotide polymorphisms in 14 genes distinguished all attenuated parasites from their virulent parental strains, all non-synonymous changes resulted in no deleterious amino acid modification that could consistently be associated with attenuation (or virulence) in this hemoparasite.
These findings indicate that chronic exposure to a HFD negatively affects the bioenergetics of liver mitochondria and this probably contributes to hypoxic stress and deleterious NO-dependent modification of mitochondrial proteins.
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