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Interestingly, PlexinA1 −/− mutants exhibit almost identical, albeit milder, phenotypes with Sema3f −/−;Sema3g lacZ/lacZ double mutants.
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Interestingly, lat-1; ten-1 double mutants exhibited almost completely penetrant developmental arrest and a greatly reduced brood size.
Nevertheless, it is impressive that the old RasGrf1 deletion mutants exhibited almost 30% lower levels of oxidized liver proteins than did the young wild-type mice.
Indeed, Scrib Crc/Crc mutants exhibited almost complete penetrance of abdominal wall defect (98%, n=50/51 at E14.5 or older), whereas less than 10% of Celsr1 Crsh/Crsh and less than 5% of Vangl2 Lp/Lp homozygotes had this defect.
Similar to the hog1Δ mutant, the hrk1Δ mutant exhibited almost complete resistance to fludioxonil, which triggers glycerol biosynthesis via the HOG pathway.
Membrane vesicles from wild-type and the KO-rev mutant exhibited almost identical response with a maximum quenching seen after addition of dNADH.
Scoring the number of cells with a bud showed that the orc5-1, fun30Δ double mutants exhibit an almost 2 fold reduction of cells with a bud, indicating a major defect in cell cycle progression, most likely because cells do not enter S phase (Figure 3 C).
In contrast, 5-day-old rab7 mutants that were raised in constant ambient light (∼600 Lux, see 'Materials and methods') exhibit almost complete loss of synaptic function.
Numerical experiments exhibit almost optimal levels of parallel efficiency.
The loops and linker regions exhibit almost no conservation.
In particular, the experiments with digitonin-permeabilized cells revealed that the UCP3R167G mutant exhibits almost normal function at high Ca2+ concentration but lacks Ca2+ uptake activity under low Ca2+ conditions.
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