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A previous study in yeast had also identified a tah18 mutant through a genetic screen for conditional tah top1T722A-hypersensitiveexhibiting exhibithermo-sensitiveitive growth at 36°C in the presence of the camptothecin mimetic mutant top1T722A [25], [26].
The first evidence of biological and physiological function of CAMTA protein was recently reported in Arabidopsis CAMTA3 (AtSR1) loss of function mutant through a reverse genetic approach [ 18].
The screen identified a muscle mutant through a highly significant reduction in birefringence, and SNP-based linkage analysis led to the identification of a nonsense mutation in tmod4.
The proportion of light output above λ=600 nm is a key determinant for transmission efficiency through mammalian tissue.[ 39] Bioluminescence data were acquired using different band-pass (bp) filters in a Photon Imager and showed that most light from the x5 Fluc mutant with 6 was collected through a λ=670 720 nm bp filter and from the x5 S284T mutant through a λ=700 750 nm bp filter.
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The expression of T3SS was upregulated in the ΔrovA mutant through an indirect regulatory mechanism, which is possibly related to the altered membrane construction in the mutant.
The observed bacterial membrane alteration was accompanied by the enhancement of T3SS expression in the ΔrovA mutant through an uncharacterized indirect mechanism.
It is interesting to note that the orientation dependence of repeat array contraction was substantially reduced in this mutant, through an increase in CTG leading-strand repeat array deletions.
In this study, we examined the activities of 20 actKR mutants through a combination of kinetic studies, PKS reconstitution, and structural analyses.
The notion was to attempt to enrich for possible mutants through a fat body insertional enhancer trap screen followed by a comprehensive longevity screen.
DOI: http://dx.doi.org/10.7554/eLife.01473.005 > -wrap-foot> We identified the sleep-altering lesion in rye mutants through a combination of recombination mapping and deep-sequencing.
Cell viability in HEK293 cultures was assessed after 72 96 h of overexpression of RUNX2-GFP or of its mutants through a colorimetric reaction, by measuring the cellular reduction of 3- 4,5-Dimethylthiazol-2-yl -2,5-Diphenyltetrazolium Bromide (MTT; Molecular Probes-Invitrogen) to formazan (44).
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