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The sod1Δ mutant has previously been shown to have a prolonged S phase (Carter et al., 2005).
This mutant has previously been shown to bind Ca2+ with kinetic properties similar to those of wild-type CaM, but was unable to activate several CaM-dependent target enzymes in vitro.
An OG1RF ΔepaB mutant has previously been reported to show reduced virulence in mice [95], higher susceptibility to phagocytic killing [71], and decreased biofilm formation compared to the wild type [71], [96].
An ohr mutant has previously been shown to be less resistant to the oxidative stress generated by 20 mM Tertiary-Butylhydroperoxide, suggesting that Ohr may be implicated in oxidative stress resistance in E. faecalis [60].
Interestingly, a lecB deficient mutant has previously been found to be significantly impaired in biofilm formation [ 26].
The loss of Rif2 in a telomerase mutant has previously been shown to promote recombination and accelerate survivor formation (Teng et al. 2000; Chang et al. 2011; Ballew and Lundblad 2013; Hu et al. 2013).
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The ΔglcD1 mutant had previously been shown to exhibit a large increase in the glycolate pool, as shown by Eisenhut et al. [15], and therefore allowed detailed analysis of glycolate labelling.
The xprG1 gain-of-function mutant had previously been shown to have the reverse phenotype to xprG - mutants with respect to extracellular protease and pigment production.
This αB-crystallin mutant had previously been shown to cause a cardiomyopathy characterized by desmin-positive protein aggregates in heterozygous humans and transgenic mice [ 187, 195].
Thus, while the phr1 mutant had previously been shown to be altered in various aspects of Pi metabolism, including Pi allocation between roots and shoots and anthocyanin accumulation, no functional implication of PHR1 in sulfur metabolism has been described [ 25, 31].
The HA-CLR mutants have previously been described (Barwell et al., 2010).
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