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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'].
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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.
The pppA-ppkA mutant cells showed increased resistance to an increased osmotic pressure caused by a high concentration of salt.
In addition, WrnΔ hel /Δ hel mutant cells exhibit increased chromosomal rearrangements with the number of passages in culture [ 22].
In a population of cells, mutant cells will increase or decrease in frequency according to the effects of the mutation on the ability of the cell to survive and reproduce.
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.
To conclude, untreated WrnΔ hel /Δ hel mutant cells exhibit increased ROS generation due to alterations in mitochondrial activities.
In intestinal mutant cells, no increase of γH2AX was detected, while DSBs were observed in a fraction of deficient ES cells.
Ofut1 mutant cells show increased Notch staining, which we have previously shown overlaps with ER markers [ 10] (see Additional file 1).
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