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Alternatively, increased epsin levels in aux mutants may result in more efficient plasma membrane localization of the remaining free clathrin.
These findings may either be explained by intra-tumor heterogeneity as suggested by Platt et al., or that the biological consequences of activating FGFR3 and RAS mutations do not overlap completely and therefore double mutants may result in an additive but small selective advantage.
These results suggest that the inviability of Hsp90 deletion mutants may result from the deficiency of Hsp90-dependent essential genes.
The lack of this age-dependent translocation in age-1(hx546) mutants may result in increased DAF-16 activity and hence explain the increased resistance to H2O2 and antioxidant activities observed in these mutants as they age [ 17, 18].
For example, the gland defects in iv37 mutants may result from specific defects in the muscles of the anterior bulb (pm4 muscles), rather than some defect localized to a specific region of the gland projection.
The increase/decrease in the distance traveled by different circadian mutants may result from either differences in time spent in motion vs. rest time, or from the differences in the velocity among the genotypes.
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Furthermore, bimolecular fluorescence complementation and co-immunoprecipitation analysis demonstrated that a substitution at 61st amino acid (His61Leu) in the tbp1 mutant may result in a reduction of the interaction between TBP1 and OsBRI1 (BR receptor in rice).
Our analyses suggest that the reduced ability to withstand stress in the im mutant may result in non-fluffy phenotype and the low degree of fiber cell wall thickness.
The significant reduction in SOD1 D83G protein is not due to allele-specific differences at the transcriptional level, but the dose-dependent decreases in SOD1 protein in heterozygous and homozygous D83G mutant mice may result from instability of mutant SOD1 and its subsequent degradation (42).
Our results suggest that long-term partial suppression of wild-type Huntingtin may be safe, and thus if a comparable level of suppression of mutant Huntingtin is beneficial, then partial suppression of both wild-type and mutant Huntingtin may result in a net benefit in patients with heterozygous Huntington's disease.
Based on our result that Gli3 (1 699), the PHS mutant form of Gli3, fails to be localized to the tips of cilia, we speculate that polydactyly in PHS patients and mutant mice may result from insufficient activation of the Gli3 repressor activity in some context.
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