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By using genetic and pharmacological approaches, we confirmed the proliferation-promoting role of ILK in vitro in gastric cancer cells.
Using gain-of-function and loss-of-function approaches we confirmed that DCD acts as a growth and survival-promoting factor in breast cancer.
By using the GST pull-down and BiFC approaches, we confirmed the interaction between OsPUB15 and PID2K in vitro and in vivo.
Next, using biochemical and genetic approaches, we confirmed the role of PKCα in regulating cancer cell morphology, the effectiveness of cancer cell invasiveness, and overall cancer cell plasticity.
By using these two approaches we confirmed the presence of a proportion of NKT cells in the PALS (∼30%) though the majority of NKT cells appear scattered around the MZ and RP of the spleen.
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Using mendelian randomisation approaches we confirm the causal role of overweight on OA.
As an alternative approach, we confirmed that cytoplasmic NADH was growth limiting in PEPCK depleted tumors by feeding the hosts ferricyanide (FeCN 22 which externally drives NADH oxidation, and this was also able to increase growth (Fig. 3c).
Using this approach, we confirmed that according to the substrates used, each pathway has a different role and consequently is otherwise involved in the partitioning of electrons through the electron transport system, and suggested that the AOX activity is triggered not only by the redox state of the cell but also by the type of substrates provided to mitochondria.
Using a more detailed approach, we confirmed these data, but we also captured substantial increase of direct costs.
Using the massively parallel bisulfite sequencing approach, we confirmed a large number of methylated genes in RL cells, and identified distinguishing methylation patterns in the promoters of these genes.
Although by using a complimentary genetic approach we confirmed that overexpression of FAK is capable of upregulating Akt phosphorylation and myofibroblast differentiation (Fig 6B), at this point, we cannot rule out an additional mechanism of action of PPAR-γ ligands that would result in reduction of Akt phosphorylation (Fig 8).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com