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In order to assess whether sulindac sulfide can activate the NF-κB pathway in the background of a variety of molecular defects, we selected three additional colorectal cancer cell lines, HCT116, SW480 and SW620.
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In the absence of a molecular defect we could not perform prenatal diagnosis.
The only molecular defects that we could provide evidence for in PIASγ-depleted cells were the inability to remove centromeric catenations and a lack of Topoisomerase II localization to centromere regions (and mitotic chromosome cores in some cells).
In this case, D4Z4 hypomethylation may impair the Polycomb recruitment that leads to a reduction in H3K27 trimethylation, the same molecular defect that we observed in contracted 4q alleles.
While the splitting into two desmosomes has been observed in Dsc3 null mice (36), breaks at the plasma membrane in correspondence to desmosome has been observed in Dsp null mice (38), consistent with the molecular defect that we observed in AEC mice.
To gain insight into the cellular and molecular defects in ap1b1 mutants, we examined the localization of basolateral membrane proteins in hair cells.
To investigate the molecular basis of the defects, we examined the mRNA levels of selected genes associated with synthesis (tpsA, tpsC and orlA) or breakdown (treA and treB) of trehalose [21] [24, Christophe d'Enfert, personal communication].
To establish whether these molecular defects compromised glucose homeostasis we first determined blood glucose levels following overnight fasting of 6- to 52-week-old mice.
Further, we enlightened the DDR in different genetic diseases, and by failure mode analysis we defined molecular defects putatively contributing to carcinogenesis.
In order to understand the molecular basis for these mitotic defects, we examined the effect of RASSF7 knockdown on established regulators of mitosis.
To investigate the molecular defect of CUL3Δ403 459, we determined whether this form of CUL3 was able to build a CRL complex.
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