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The variants were resistant to inhibition by nerve agent model compounds of soman (i.e., SPGD3N), sarin (i.e., SPGB3N), and cyclosarin (i.e., SPGF3N).
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Furthermore, these variants are resistant to the RNAi, potentially by stoichiometrically overwhelming this cellular mechanism.
Together, our data demonstrate that hinge domain null AR splicing variants are resistant to SPOP-mediated degradation.
In contrast to WT IGFBP-2, the PR variant was resistant to proteolysis by proteases present in T84, SW480 and MCF-7 CM.
Figure 1D and Table 2 shows that while the DLKPA variant is resistant to docetaxel, both parent cell line DLKP and its drug-resistant variant DLKPA are equally sensitive to EL102.
The antibiotic susceptibilityshowed the KP producing novel KPC variant was resistant to most of the antibiotics, such as carbapenem (imipenem, ertapenem and meropenem), aztreonam, cephalosporin (cefazolin, cefotaxime and ceftazidime), but susceptible to amikacin and colistin.
MTCT resulted in selection for variants that were resistant to maternal antibodies, suggesting that maternal antibodies can protect the baby from those variants that are susceptible to the antibodies present.
The d-amino acid variants were fully resistant to proteolysis by trypsin and bacterial proteases.
Although some amyloidogenic TTR variants were apparently resistant to proteolysis (Mangione et al, 2014), we have shown here that susceptibility to proteolytic cleavage is enhanced by increasing shear stress.
Accordingly, both I56F and S68A variants were relatively resistant to the inhibition by MitoVES and to cell death induced by this agent, whereas the S68A variant, which is more efficiently inhibited by TTFA, underwent proportionally higher level of cell death upon TTFA treatment.
Because work with actual nerve agents is precluded in most academic laboratories, we developed a series of nerve agent model compounds that were used to identify variants of hBChE that were resistant to inhibition by these compounds.
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