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In contrast, 13 mutants lost the ability to interact with both partners.
Neither the P-loop mutant (G221R) nor the coiled-coil deletion (ΔCC) were able to bind the LeEix2 receptor, and both mutants lost the ability to inhibit HR.
Since all of these mutants lost the ability to be secreted, we hypothesize that a change on the surface, if not causing misfolding, should interfere with the secretion process, e.g. hampering attachment of the protein to the membrane.
When the class averages of 6,000 particles obtained from membranes of the pilF and pilE deletion mutants without (Figure 5G and 5I) and with applied symmetry (Figure 5H and 5J) were compared to the class averages obtained from wild-type membranes, it appeared that the secretin structures of both mutants lost the extending spike-like densities.
All 4 mutants lost the DNA binding activity.
Our results showed that BZcon1 was directly involved in activating the development of conidiophores, because the BZcon1 mutants lost the conidia production capacity.
Similar(52)
Therefore, the Thr564Ala and Ser582Ala mutants lose the binding ability to 8H3 due to the collapse of dimeric form of E2s.
The ΔrovA mutants losing the backbone of the suicide vector were counter-selected on LB plates with 5% sucrose.
For example, mutator mutants lose the mismatch repair system [ 1], which affects the entire genome.
PHD mutants lose the ability to undergo cellular senescence linking chromatin mark recognition with cellular senescence.
Mutation spectra analyses showed that the ratio of λ mutants losing the redBA/ gam region induced by chrysotiles was similar to those induced by equitoxic doses of H2O2.
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