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Exact(5)
Moreover, the similarity of the behavior of R105W mutant and cystein mutants suggests that the lack of secretion observed with the naturally occurring mutant could result from impaired disulfide bond formation.
Their low level expression in the mutant could result in uncontrolled PCD, contributing to the susceptibility.
The increased persistence exhibited by the SO2 phoP mutant could result in prolonged exposure to the immune system and consequently in long-term immunogenicity.
Flow cytometry analysis confirmed that all RIP3 proteins were expressed with a slightly lower level for RIP3-KD, ruling out the possibility that the increased death rates observed for this mutant could result from enhanced expression levels.
The high Δ Ψ in the sir2Δ mutant could result from at least two distinct mechanisms: decreased activity of the potassium uptake system (Madrid et al., 1998) or increased expression of PMA1, which encodes a plasma membrane H+-ATPase (Serrano et al., 1986).
Similar(55)
In light of this hypothesis, it was possible to conceive that some of the defects in polyglycylation, observed in Bug22 mutants could result from defects in IC migration.
Gland defects in sma-1 mutants could result either from structural defects in the gland themselves or from defects in the surrounding pharyngeal muscles.
Thus, it is plausible that the slight increase in γH2Av in His C mutants could result from incomplete turnover of γH2Av rather than directly reflect DNA damage that could activate the S phase checkpoints.
Here, the increase in phenotypic heterogeneity that probably occurred through transcriptional-mediated noise in gene expression was a relevant evolutionary strategy because the larger distribution of the more variable mutants could result in a similar survival probability than for mutants with increased mean and narrow distribution.
Although eat-4 ky5) eat-4 ky5id not show locomutantsdidect, they dispersed less thanotild-type animalshow the absence of a temperature gradient (SupplocomotionFigure S2A andefectégalathey al, 1995), indispersedthe possibiless than abnormal TTX indices of eat-4(ky5) mutants could result from other defects, such as local search defect.
Although loss of function in mutants could result from protein misfolding, these results are consistent with an arginine residue being required at position 219 for uptake of MAs III) and suggest that MAs III) shares the same channel pathway as As III) and glycerol.
Related(20)
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