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Previous studies have shown that there were potentially pathogenic variants co-segregated with the primary LHON mutation and enhanced the clinical expression of LHON [34], [35].
Here we simulated epistatic datasets which are not constrained to specific predetermined models but instead achieve a diversity of gene-disease relationships created by the randomness of mutation and enhanced through the model-agnostic selective power of evolution.
In this study, we demonstrated that the F309S mutation and enhanced B-domain glycosylations alone are not sufficient to improve FVIII HC secretion, which suggested a role of the FVIII LC in regulating HC secretion.
Both mutation and enhanced expression of RAS genes have been reported in AML [32].
SSAs and MSI cancers were reported to exhibit similar features including predominant location in the proximal colon, high BRAF and low KRAS mutation and enhanced DNA hypermethylation [ 12- 17].
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Compared to unlinked mutations, G is reduced for beneficial mutations and enhanced for deleterious mutations.
The biological consequences of CFTR mutations are numerous, and two main types of drugs have been investigated to correct these effects: the potentiators and correctors that increase ion flow (class III and IV mutations) and enhance productive trafficking (class II mutations), respectively [52, 53].
Recombination may also accelerate the accumulation of mutations and enhance viral diversification (see below) [32].
Overexpression of BnNPR1 from canola and OsiNPR1/NH1 in rice complement the npr1 mutations and enhance resistance [ 23, 46, 47].
This term is also used more broadly to describe the interplay between linkage and selection: interference interactions reduce the fixation probability of beneficial mutations and enhance that of deleterious ones.
Although Tau and α-Syn have distinct biological functions, in vitro studies have shown that α-Syn can induce fibrillization of Tau, and vice versa, with the A53T mutation accelerating and enhancing formation of fibrils as compared to wildtype α-Syn [12].
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