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The catalytic domain only mutants have lost their preference for tyrosine (Fig. 4C).
Because odr-7 mutants are, if anything, enhanced in their responses to cyclohexanone and ceh-36 mutants have lost cyclohexanone responsiveness, we conclude that AWC is the predominant cellular origin of cyclohexanone responsiveness.
Charcot Marie Tooth disease-associated GDAP1 mutants have lost this protective effect, thereby providing a hint that the disease might be linked to oxidative stress (Noack et al., 2012).
Tu et al. (32) reported that the C-terminal region of HBx is crucial to its transcriptional function and that, in tumor tissues, most HBx natural mutants have lost their capacity for controlling cell proliferation, viability and transformation.
We are neither suggesting that the propensity of αSynuclein to aggregate is the only property nor that it is the main property of the protein causing DA neurodegeneration, but our results clearly indicate that aggregation plays a major role in the progression of DA cell loss and that aggregation-impaired mutants have lost the ability to trigger a sustained neurodegeneration.
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Eleven of the Mel− mutants had lost the melC sequence (Southern hybridization data not shown).
Analysis of the eight ura4+ insertion mutants by PCR revealed that seven mutants had lost their barcodes, indicating that successful integration was frequently accompanied by deletion of barcodes.
In contrast, only 4 of 30 (13.3%) of mutants derived from cells exposed to DPE (20 μg/mL) + UVA (0.5 J/ cm) retained all the marker genes examined, whereas 26 of 30 (86.7%) of the mutants had lost at least one additional marker, which included 8 of 30 (26.7%) that lost the proximal APO-A1 located on the long arm of the chromosome.
These observations suggest that the H486R mutant has lost the ability to inhibit NF-κB activation induced by TNFα.
Interestingly, at these two pH values, the Asp282-Cys283 peptide bond in the H251A mutant was maintained in cis, but in the H284A mutant, this peptide bond was in trans, indicating that the H251A mutant still retained GlcNAc binding activity, but the H284A mutant has lost its binding activity for GlcNAc (Table 2).
At day 5 post-inoculation, mice infected with the sigS mutant had lost on average only 4.4% (−13.3% to +2.2%, IQR) of their body weight, whereas SH1000 infected mice had a median weight loss of 10.4% (−20.2% to −5%, IQR) (p<0.05, Fig. 6B).
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