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The average size of mutant cells increased over time to 32.43 µm (n = 79) at the completion of 20 rounds of growth, while size of control cells did not change.
Although levels of secreted VEGF did not differ significantly between wild-type and mutant EGFR cell lines when grown in vitro under normoxic conditions, following exposure to 0.1% hypoxia levels of VEGF produced by mutant cells increased 3.5 6.6 fold compared to 2 or less for full length EGFR cells.
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The result that an increased migration potential of mutant cells increases their ability to invade, can be explained intuitively.
Co-localization of NICD and Hrs in awd mutant cells increases by the over-expression of Rab5CA [see Additional file 9: Figure S9B compared to Additional file 5: Figure S5B'].
Although less p53 induction was observed in TP53 mutant Daoy cells, increased TP73 levels including ΔN'p73 were detected.
We found that, although the relative Aβ42 levels in CSF decreased in most of the cases, the relative APL1β28 levels in CSF and the relative APL1β28 generation by mutant-expressing cells increased in parallel.
The pppA-ppkA mutant cells showed increased resistance to an increased osmotic pressure caused by a high concentration of salt.
We noted that in Figure 1b, co-transfection of ΔNp63 α with the more active ΔSH3 c-Abl mutant in 293 cells increased its protein stability relative to co-expression with the less active full-length c-Abl.
Transfection of S21 A/D eEF1A mutants in H1355 cells increased apoptosis in comparison with the wt isoforms.
We also noted that dpoA mutant cells exhibited increased speed of movement in control conditions, treatment with NaCl, suggesting that DpoA suppresses this aspect of the chemotaxis response.
In addition, WrnΔ hel /Δ hel mutant cells exhibit increased chromosomal rearrangements with the number of passages in culture [ 22].
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