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Next, we questioned how JNK controls the activity of Cdk1.
Next, we questioned whether the H19 message affects tumor growth of other cell lineages.
Next, we questioned if dimerization or truncation is important for cytokine-like activity.
Next, we questioned the effect of HP diet in mice with deletion of the POMC gene.
Next, we questioned whether H19 RNA is a tumor-associated gene product or whether it is potentially harboring an oncogenic potential by itself.
Next, we questioned whether the rapid downregulation of ERα levels in GH3 cells by ICI is mediated through the ubiquitin-proteasome system.
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As we revealed here that hTERT could be phosphorylated by BCR-ABL, we next questioned whether BCR-ABL could also govern hTERT translocation in different cellular compartments.
We next questioned whether the pathway is active in the developing brain.
We next questioned whether direct intervention in the interleukin-STAT3 axis could revert the up-regulation of PD-L1 by BCG.
We next questioned whether the effects of the GPR120 activation also occurred in adipocytes that had differentiated to a beige phenotype.
We next questioned whether the CPP would preferentially inhibit tumour cell growth while sparing normal cells.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com