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We lastly confirmed the Lck specific cytotoxicity of long peptide‐induced CTL with HLA‐A2+ Lck− cancer cells (LNCaP), HLA‐A2+ Lck+ cancer cells (SW620) and HLA‐A2− Lck+ cells (SQ‐1) as target cells.
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Lastly, we confirmed these results using immunogold labeling and electron microscopy (EM).
Lastly, we confirmed that NOSTRIN expression could be a good prognosticator.
Lastly, we confirmed that Tomato+ cells were not Sox2+ NPs (Figs. 5M O).
Lastly, we confirmed that the adenosine-dependent regulation of KCa3.1 was relevant to KCa3.1 channels that had been opened by anti-IgE-dependent activation.
Lastly, we confirmed that lack of Prdx1 enhanced basal and H2O2-induced phosphorylation of Akt substrates in Prdx1−/−MEFs more than in Prdx1+/+MEFs.
Lastly, we confirmed whether PGE2-dependent regulation of KCa3.1 was relevant to KCa3.1 channels that had been opened by anti-IgE-dependent activation.
Lastly, we confirmed that IL-1 β plays a role in expression of proinflammatory mediators, IL-6 and IL-8, via the IL-1 receptor suggesting that BRAT might stimulate a proinflammatory environment that could promote OC oncogenesis.
Lastly, we confirmed that the increase in LC3 flux observed in young L2AKO was no longer evident in 12-month-old L2AKO mice, which even displayed a trend toward lower flux than Ctr mice (Fig. 6B).
Lastly, we confirmed that when human NK cells were exposed to a similar cytokine environment as was observed in IL-15 TG/MT tumors, they were capable of killing human breast tumor cells.
Lastly, we confirmed that the functional expression of TRAIL-R2 was the essential mechanism of sensitization of #63 cells to TRAIL by genotoxic agents using antagonistic anti-TRAIL-R2 Ab.
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