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We have further elucidated that the inhibition of NSPC proliferation by CM from BV2 results from a blockade of cell cycle progression mainly at G1→S phase due to the upregulation of various checkpoint proteins.
Blockade of cell cycle progression and downregulation of fanconi anemia group D2 (FANCD2) were implicated in the anti-tumor mechanism of curcumin [ 277].
One distinctive feature of cancer cells is their sustained proliferative activity; thus blockade of cell cycle is regarded as effective strategy for cancer therapy [ 14].
Also, TN-mediated inhibition of cell proliferation has been markedly associated with blockade of cell cycle progression and consequent cell arrest in the G0/ G1 transition [ 58, 59, 164, 169].
Flow cytometric DNA analysis of MIA PaCa-2 cells incubated with EPA demonstrated the presence of sub G1 populations corresponding to the presence of apoptotic cells and the blockade of cell cycle progression in S-phase and G2/M-phase.
Yano et al. [ 36] investigated the anti-proliferative effects of IFN in 13 human HCC cell lines and reported blockade of cell cycle at S-phase in 11 of 13 cell lines.
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The major new finding reported here is that the effect of PI3K/mTOR blockade on cell cycle progression in MM cells is critically dependent on the underlying mode of cyclin D dysregulation, which in turn is dictated by IgH translocation status.
Thus, the differential impact of PI3K/mTOR blockade on cell cycle progression between cyclin D2-expressing t(4 14) or t(14 16) and cyclin D1-expressing t(11 14) MM tumours may be due to the composition and activity of cyclin D CDK complexes, and their regulation by proteolytic mechanisms.
These results collectively indicate that the addition of C26 CM inhibited myoblast proliferation through pRb-mediated blockade of cell-cycle progression at the G0/G1 checkpoint.
Initial cell killing and blockade of cell-cycle progression (0-24 h) was followed by recovery of proliferation due to recruitment of cells from the non-proliferative compartment, cell cycle and phase times remaining unaltered.
Both the cytotoxic and cytokinetic results revealed that the growth-inhibition by H-8 of P388 cells is mainly due to a blockade of cell-cycle progression rather than due to a killing of cells.
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