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Some mutants had very low level of fibrilization (very low plateau height) (e.g. the F3/A mutant), which may explain the absence of β-sheet conformation by CD for these mutants.
This will allow definition of the overall profile of deficits across multiple systems in each individual mutant, which may be quite unique.
Importantly, AMPKαSsp2 levels were reduced in the AMPKβ amk2.Δ AMPKγ cbs2.Δ double mutant, which may account for the slight delay in the response of this mutant to nitrogen stress.
The lack of a dramatic gain-of-function phenotype in the MPN-BSH mp-S319 plants may be attributable to the residual MP activity present in the hypomorph mp-S319 mutant, which may interpret the auxin gradient.
The increased separation between the OH of Y237 and the hydroxyethyl moiety of heme a3 results in a loss of the hydrogen bonding interaction in the G232V mutant, which may affect proton-coupled electron transfer involving the cross-linked tyrosine in the mixed valence mutant and/or disrupt the K proton channel.
As is discussed in the following section, SAK1 expression monitored by qRT-PCR followed the latter trend as the 5′UTR of the gene was elevated in the mutant, which may be a result of response to other factors such as a possible oxidization product of O2.
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Yet, both immunocompetent and immunocompromised individuals could generate high viral loads of single and double mutants, which may facilitate their onward transmission and the subsequent accumulation of additional 1 2 mutations in newly-infected individuals.
These structural features of the intermediate components can be related to a less tightly controlled biosynthesis of the branching structures in high-amylose maize starch mutants, which may prevent these molecules from maturing into full-size amylopectin.
Thus, similarly to the acetyl-CoA transporter, more than one process is impaired in sdh1Δ mutants, which may compromise lifespan.
Therefore, the effects of a gene may be underestimated by simply analyzing the hypomorphic mutants, which may lead to an underestimation in the effects of a gene.
One potential problem associated with anti-HIV therapy is the emergence of resistant mutants, which may ultimately render the currently available highly active antiretroviral therapy (HAART) ineffective [ 58– 60].
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