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Overall, these data suggest that tighter binding of lead by the isozymes of the ALAD2 allele decreases lead sequestration in bone.
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We postulate that the enhanced cytoplasmic localization of isoform 2 might lead to sequestration of active Rac1 in the cytoplasm, thus leading to lower levels of active Rac1 near plasma membrane and thus lower macropinocytosis.
Thus, excess LMO2 rather than an intrinsically higher binding affinity would lead to sequestration of Ldb1.
Release of CC from NE formulations was faster at Smix concentration percent lower than 36% and this is may be attributed to the fact that the high Smix concentration may lead to sequestration of the drug into the surfactant micelles or emulsified cinnamon oil droplets and delay the release of the drug via the dialysis bag (Sainsbury et al. 2014).
The presence of additional microRNA regulated mRNA could lead to sequestration of mir122 molecules away from their endogenous targets.
Such an interaction could lead to sequestration of the available pools of FtsZ required for catalyzing Z-ring assembly and cell division in M. tuberculosis.
This could lead to sequestration of the microRNA away from its endogenous mRNA targets and alter the expression patterns of many genes.
Whereas in M-Phase, all γ-H2AX was located along the condensed chromosomes with no cytoplasmic signal, the other phosphorylated proteins remained in the cytoplasm and did not co-locate with the chromatin indicating that 32Hc-activated DNA-PK does not lead to sequestration of the target proteins at a specific locus (Fig. 3D).
Furthermore, the formation of synphilin-1 aggresomes may also lead to sequestration of noxious forms of α-Syn, thereby providing an alternative to deal with this protein as well, on condition that the overall capacity for aggresome formation is not exceeded.
Drugs which inhibit endosomal recycling lead to sequestration of these proteins in vesicles of the endosomal pathway [ 29, 30].
Such desensitization is typically initiated by GPCR phosphorylation, uncoupling the receptor from its cognate G-protein, and may lead to sequestration and internalization of the desensitized GPCR from the plasma membrane into intracellular compartments [18,19].
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