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ART, DHA, and AS remarkably inhibited the proliferation of human NSCLC A549 and H1299 cells by arresting cell cycle in G1 phase.
Although these analogues differ in their formulation and bioavailability, the mechanism of inhibition is the same, binding to the mTORC1 target, thereby arresting cell cycling at the G1 phase.
Preliminary mechanism research on one of the most potent compound 6p indicated that it was a potent tubulin polymerization inhibitor, with IC50 value of 3.8 μM, equivalent to that of CA-4, and arresting cell cycle in G2/M phase.
In view of the importance of picolinic acid (PA) in preventing cell growth and arresting cell cycle, new PA based metallonucleases were designed with a view to study their DNA binding and cleavage abilities.
Primary mechanism research on the most potent compound 6f indicated that it was a potent tubulin polymerization inhibitor, with IC50 value of 4.3 μM, equivalent to that of CA-4, and arresting cell cycle in G2/M phase.
Two of the most potent compounds, 68 and 75, effectively suppress PC-3 cell proliferation by activating cell apoptosis and by arresting cell cycle in the G0/G1 phase.
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Moreover, knockdown of chondroitin inhibited cell proliferation and migration, as well as arresting cells in the G2/M phase.
In addition, suppression of CDCA3 expression with shRNA significantly (p < 0.05) inhibited cellular proliferation compared with the control cells by arresting cell-cycle progression at the G1 phase.
In addition, resveratrol was found in a high-throughput screen for the identification of Notch activating compounds using carcinoid cell lines [ 102], and treatment of thyroid carcinoma cells with resveratrol was shown to inhibit growth by arresting cell-cycle progression in the S-phase and induce Notch protein expression and signaling by transcriptional regulation [ 103, 104].
The anti-proliferation effect of IKKε siRNA is mediated by arresting cells in the G0/G1 phase.
More importantly, ART even can arrest cell cycle of multidrug-resistant retinoblastoma cells [117].
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