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Alamar Blue (Invitrogen), a dye used to detect metabolic activity in cells, was used to assay for cell viability and to identify genes that alter paclitaxel sensitivity.
After four days of drug treatment, cell viability was measured using an Alamar Blue assay to identify genes that alter paclitaxel sensitivity (effect of shRNA and drug).
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Modulating miR-9 expression could change paclitaxel sensitivity of EOC cells.
In contrast, cepharanthine does not significantly alter paclitaxel transport in empty vector-transfected HEK293 cells.
Bioinformatic tools were applied to understand how these genetic variants alter paclitaxel response.
Thus, the missense substitution caused by BTBD12's variant could reduce its DNA repair ability leading to increased paclitaxel susceptibility or alter paclitaxel's ability to arrest mitosis.
Nevertheless, our analysis suggested that the genes identified here fall into two groups: those altering paclitaxel response through the β-catenin and p53 transcriptional regulatory axis, and those altering paclitaxel response through microtubule interactions.
Furthermore, specific β-tubulin mutations that alter sensitivity to paclitaxel have been reported in vitro [ 75– 75].
Considering the potential of EB1 as a marker to predict paclitaxel sensitivity or as a target to increase paclitaxel sensitivity, the molecular mechanism of how EB1 regulates paclitaxel sensitivity merits further investigation.
We then sought to investigate the molecular mechanism of how EB1 regulates paclitaxel sensitivity.
In vitro cell proliferation assays reveal that EB1 stimulates paclitaxel sensitivity in breast cancer cell lines.
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