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Because it has also been demonstrated that a low gastric pH is required for absorption of dietary iron [9], we hypothesize that the increased gastric pH in Kcne2 tmutantsa mutants could account for the low plasma iron and iron-deficient anemia.
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The increased expression of ICL in the phoP mutant could account for the persistent phenotype displayed by this strain upon infection of BALB/c mice (Figure 7).
Because hydrogen bonding is considered to directly influence protein thermostability [ 34], we hypothesize that additional hydrogen bonding in the Q10Y mutant could account for its increased thermostability.
Therefore, differences between Z1 and Z4 are evident at the L1 stage in hnd-1 mutants and could account for the higher percentage of missing anterior gonadal arms.
2) Much of the data is shown at low magnification and lacks cellular resolution: In Figure 2A melanophores appear smaller in Tjp1a mutants, which could account for altered behaviors of iridophores.
The extensive Dido3 truncation in the Dido3ΔCT-RFP mutant might exacerbate the effects observed after partial Dido inactivation in the Dido3ΔNT mutant, which could account for impaired stem cell differentiation, developmental defects and early embryonic lethality in Dido3ΔCT-RFP mice.
Differences in expression levels of the mutant protein could account for these discrepancies.
To find out if the predicted instability of mutant Gigaxonins could account for the decreased abundance of Gigaxonin in patients, we determined the half-lives of wild type and mutated Gigaxonin.
Thus, our experimental results demonstrate that the D1 amino acid substitutions responsible for the radiation tolerance in the random mutants, could also account for the improved resistance under high light exposure of the site-directed mutants.
Glutamate is a prominent constituent of peptidoglycan; thus, disruption of its uptake in the proteobacterial mce operon mutants could perhaps account for the observed effect on cell envelope properties.
The L er allele of the QTL shortened the circadian period by 0.8 h, as did independent flc mutant alleles, leading us to conclude that the known allelic variation in FLC could account for the QTL [ 10].
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