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Moreover, Lim et al. reported that direct conversion into iHeps is a stepwise transition involving the sequential erasure of somatic memory, MET transition, and induction of hepatic cell fate (Lim et al., 2016).
Moreover, stable, long-term expression of a dominant-negative EGFR leads to a mesenchymal to epithelial-like transition and induction of angiogenic tumor growth.
There are some studies that indicated that MSCs have protumorigenic capacity due to their immunosuppression properties, modulation of the epithelial-to-mesenchymal transition, and induction of angiogenesis [ 36].
Collectively, these results imply that TGFBI plays a suppressive role in the development of mesothelioma and breast cancer cells, possibly through inhibitions of cell proliferation, delaying of G1-S phase transition, and induction of senescence.
We provide evidence to support this chain of biochemical and cellular events after PFKFB3 inhibition as well as direct verification that p27 itself is required for the simultaneous suppression of G1/S transition and induction of apoptosis caused by PFKFB3 inhibition.
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Importantly, whereas p27 siRNA transfection had no effect on the cell cycle or apoptosis, we found that the p27 siRNA resulted in near complete reversal of the G1/S transition block and induction of apoptosis caused by PFKFB3 siRNA transfection.
[Ca2+]i transients are required for the proliferative cell cycle to progress, including the G1/S-phase transition, S-phase, and mitosis, as well as key points within mitosis such as the metaphase-anaphase transition and the induction of cytokinesis.
The cell cycle control is predominantly controlled at the G1/S transition and the induction of positive factors and deregulation of negative factors that regulate cell cycle progression may cause an imbalance in this transition, leading to malignant transformation (Weinberg, 1989).
The decrease in the number of viable BT-20 cells upon PARP-1 inhibition was associated with the strong accumulation of cells arrested at the G2/M transition and concomitant induction of caspase-dependent apoptosis.
The apparent activation energy values for induction and transition between induction and growth were calculated by the Arrhenius equation resulting in values of 58 and 21 kJ/mol, respectively.
Together, this set of experiments shows that Bortezomib impairs Taxol-induced G2/M transition, mitotic arrest and induction of polyploidy.
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