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Further biochemical evaluation and cocrystal structures with tubulin demonstrated that both compounds disrupted tubulin polymerization through interacting at the colchicine-binding site, suppressed angiogenesis in vitro and in vivo, blocked cell cycle progression at mitotic phase and induced cellular apoptosis.
Treatment with zeocin from the beginning of the cell cycle blocked cell cycle progression in G2 phase with duplicated DNA.
CifBp also blocked cell cycle progression, as demonstrated by the accumulation of G2 arrested cells containing 4N DNA content (Fig. 4B).
Incubation of LAN-5 with antagomir-17-5p, but not with the control antagomir, markedly inhibited cell proliferation, decreased in vitro tumorigenesis in soft agar and blocked cell cycle progression (Figure 4A, B and data not shown).
Knockdown of CNDP2 inhibited cell proliferation, blocked cell cycle progression and retarded carcinogenesis in an animal model.
In this study, we found that FOXO transcription factors blocked cell cycle progression at the G1 phase through the regulation of p27 and p21.
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The microtubule targeting compounds engage at the mitotic spindle checkpoint where they block cell cycle progression at mitosis ultimately leading to apoptosis (Bhat and Setaluri [2007]).
Checkpoint kinase 1 (ChK1) is activated in response to DNA damage, acting to temporarily block cell cycle progression and allow for DNA repair.
At the concentration that can block cell cycle progression and DNA synthesis but not elicit apoptosis, these inhibitors potentiate FasL to induce apoptosis.
The use of antimitotic substances, such as colchicine, promotes depolymerization of microtubules and prevents the formation of spindle fibers, this methodology is used to block cell cycle progression and thus induce polyploidy (Pereira et al. [2012]).
Therefore, it was concluded that L-4 can inhibit the proliferation of EC109 cells via blocking cell cycle progression and inducing reactive oxygen species-dependent and mitochondria-mediated apoptosis.
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