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Overexpression of this mutant leads to a dramatic change in cell morphology, with the appearance of large early endocytic structures.
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This mutant led to increased production of not only resveratrol but also the flavonoid naringenin, when introduced in their corresponding biosynthetic pathways.
This mutant led to the unexpected finding that inactivating the uptake hydrogenase in Cyanothece 7822 lowered H2 evolution and nitrogenase activity, thus demonstrating the importance of HupLS in protecting nitrogenase from O2 toxicity.
The expression of this particular mutant leads to smaller mitochondria compared with that of non-treated cells transfected with empty control vectors, in accordance with previous reports (Fig. 7A and B) (46, 93).
The PTEN-related protein TPTE, which normally lacks any detectable lipid and protein phosphatase activity, can be reactivated through mutation, and only this reactivated mutant leads to nondirectional migration of these cells in vivo.
Surprisingly, infection with the mutant led to a faster killing in the systemic model of infection.
Expression of NvHoxB or NvHoxE in this mutant context leads to a complete or strong rescue of this phenotype, respectively.
This showed that the introduction of the two hypotheses for the clv1-1 mutant leads to differences in the properties of the unperturbed stem cell regulating network.
Conversely, expression of any of the mutants leads to a decrease in levels of the downstream genes tested except tbx1.
In other words, transfection with these mutants leads to a degradation of unincorporated Pen-2 quicker than that with the wild type.
Deletion of GAP1 in these mutants leads to loss of FLO11 expression and a planktonic form, revealing that Gap1p can regulate biofilm formation via FLO11.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com