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In order to avoid any effect of glucose on cell death we chose to stimulate the INS-1E cells with 5 mM glucose instead of 11 mM glucose in the DEDTC experiment because our data indicated that 11 mM tended to affect the necrotic state of INS-1E cells (data not shown).
Because our data indicated decreased hypoxia in platelet-depleted tumors, we considered the possible involvement of growth factors known to regulate tumor growth and metastasis.
The second session from each day was selected because our data indicated that the first session may not be valid and, therefore, should represent practice trials.
Second, C-ion irradiation may be advantageous in the induction of truncation mutants rather than generation of allelic series, because our data indicated that small indel mutations occurred more frequently than base-change mutations.
Because our data indicated that IL-13 signaling induces TP63 expression and that IL13Rα2 depletion enhances IL-13-mediated STAT6 phosphorylation, we hypothesized that TP63 upregulation could be linked to STAT6 activation.
Because our data indicated that GDF15 increased Kv2.1 protein synthesis and prevented its degradation, we first tried to determine whether the Akt/mTOR pathway, which has been reported to affect protein synthesis and CGN mutation [ 17, 23], was activated by GDF15.
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Because our data indicate that ApoEr2 plays an important role in promoting synapse and dendritic spine numbers, we examined whether ApoEr2 affects clustering of synaptic proteins.
Because our data indicate that enz acts cell autonomously, enz would be predicted to be a downstream effector if it acts in such a hormonal signaling pathway.
Because our data indicate that ELT-2 regulates a multi-pathogen immune response, we studied whether the transcription factor is required for the effects of DAF-2 in immunity to pathogens.
Because our data indicate that these various null alleles are equivalent, we refer to them without individual allelic designations henceforth (nf1a−/− and nf1b−/−).
However, because our data indicate that neither Rep nor UvrD act on R-loops in Inv mutants, the synergistic effects of inactivating dinG in rep or uvrD mutants indicate that R-loops are not the only target of DinG.
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