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Compared with the parental cell line of BSC-1, ts13 and ts14 cells were blocked in the G1 phase of the cell cycle during the time that the cell were in contact with the carcinogen (MNU); the variant cells also had higher mitotic indices at this time.
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H69/41d cells have a distinct morphology: while H69 cells are non-adherent cells that form ragged aggregates, the variant cells, while also non-adherent, form tight spheres reminiscent of those seen with stem cell populations (Figure 5A).
Except for the splice variant TβRIB, PC-3 cells also expressed all receptor splice variants, whereas LNCaP cells did not express TGF-β2B which is in line with the missing expression of all TGF-β ligands.
Similarly, 2.7hPLPΔ3874 5810 transfected cells also expressed splice variants containing all or just a part of exon AB (A portion), but not hPLP C-related splice variants as exon C is missing from this construct.
It is possible that MCF-7 cells also express other VGSC α subunit variants that have impaired conduction [ 48].
ATG16L1300A/300A cells also displayed significantly reduced CFUs compared to HCT116 cells indicating that the ATG16L1 T300A variant may reduce bacterial invasion into these cells.
This variant was also internalized by A431 cells, likely via receptor-mediated endocytosis, and it efficiently inhibited EGF-mediated tyrosine phosphorylation of the EGFR.
This short variant was also strongly present in HepG2 cells, and detectable at low intensity in MDA-MB 321 cells.
This is in accord with the observation that both C1 variants cloned from HME cells were also cloned from SUM-52PE cells.
However, other mechanisms of bacterial latency such as phenotypic variants leading to persister cells have also been described [ 1], and are increasingly encountered in the clinic.
Cells expressing the variant Bcl-xL also continued to proliferate and showed increased viable cell numbers following gradual serum withdrawal.
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