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Some labs have reported that at least one of the RS domains of SF2/ASF and U1-70K is required for interactions between these two proteins [13], [67], but these experiments did not demonstrate that the RS domains of both proteins were required for their interaction.
Previously, we found that RSSs are preferentially protected by a nucleosome (Baumann et al, 2003) but these experiments did not distinguish where the RSS lies with respect to the histone octamer.
Multi-site phosphorylation has been elegantly studied in the TGFβ signaling axis using protein semisynthesis previously (Huse et al., 2001; Wu et al., 2001), but these experiments did not require insect cell expression of an intein-fusion protein.
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Previous studies attempted to estimate the impedance by recording force as a result of position perturbations, but these experiments do not require a feasible task of human beings.
But these experiments don't definitively prove that NS1 is the culprit, the human and pig immune systems might react differently to it.
We see what happens but these experiments do not probe how it happens.
Studies conducted in our laboratory with the innervated rabbit heart show that the protective effect of VNS is not dependent upon the brain, but these experiments do not exclude the existence of additional anti-arrhythmic mechanisms in vivo or afferent reflex responses which can occur locally [ 38].
These experiments did not always work.
These experiments did not result in SiC or equilibrium assemblages.
These materials include the bulk of the solid cellular material, the intracellular water and water-soluble cellular components, but, importantly for these experiments, do not include the starch-rich statoliths within the cells.
An answer to that question is beyond the scope of this paper, but the results of these experiments do provide a roadmap for future investigation into their relationship to the clinical situation we are trying to model.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com