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This defect is due to two mutations that arose in an ancestor of most teleost fish, implying that most fish lack effective RNAi.
It is a formation defect; the necessity to classify it in a different class than that of aplastic uterus (formation defect) is due to the existence of a fully developed functional uterine hemicavity.
Intriguingly, Johnson et al also found that the TLR1 signaling defect is due to a complete absence of TLR1 on the surface of monocytes in GG individuals [38].
It was presumed that this virulence defect is due to increased DNA damage in the recA mutant mediated by ROS produced by macrophages.
OPT1 and YJL211c are adjacent to, or overlap with, PEX2 respectively, raising the possibility that the opt1Δ mislocalization defect is due to disruption of PEX2.
Thus, it is not clear whether this virulence defect is due to specific sensitivity to phagocytic ROS, or is a nonspecific effect caused by the altered growth rate of the mutant.
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This defect was due to a gradual, age dependent disorganization of the sarcomeric actin, Z-line, and M-line.
This finding confirmed that the lactation defect was due to the deletion of Ndst1 specifically in the mammary epithelia.
Since tomm-40 was ubiquitously expressed, we asked if the observed growth defect was due to any pharyngeal or intestinal defects, which would cause feeding defects.
In order to confirm that the Mys localisation defect was due to a lack of Rac1 signalling, we overexpressed Rac1 in a homozygous Rac1J11 background [26], [28].
We next wished to investigate whether the DAF-28 secretion defect was due to secondary effects of the mitochondrial inactivation, or due to a neuron specific effect, since neurons are refractory to feeding RNAi against some genes [36].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com