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A possible interpretation of our data might be that induction of G1-S cyclins by Ras eventually counteracts the p53-dependent proliferative block, leading to re-entry into the cell cycle and cell transformation.
One explanation might be that induction of apoptosis upon TQ might depend on Msh2.
It may be that induction of pyrimidine-salvage genes could represent a signal for insufficient levels of nucleotides, thus preventing cells from undergoing a round of DNA replication.
Thus an alternative benefit of the observed changes could be that induction of VSP and GLS production assists the plant in managing a nutrient imbalance that occurs as a result of K-deficiency.
Because undifferentiated and differentiated germ cells are intermixed in the human and there is no defined "early" or "late" period in terms of germ cell differentiation, it may be that induction of aggregation in the human is simply less possible, as opposed to the rodent fetal testes where germ cell differentiation occurs synchronously (McKinnell et al. 2013; Mitchell et al. 2010).
Similar(55)
A striking feature of our data is that induction of FGF2 protein is concomitant with a decrease in FGF2 mRNA, in vivo.
An additional finding that could be inferred from our data is that induction of gene transcription, compared with inhibition, was the common response among those genes most frequently regulated by BMP4 and BMP7 in breast cancer cells.
Thus, the model that emerges from our results is that induction of apoptosis leads to a rapid rise in mitochondrial membrane potential and the generation of intramitochondrial ROS, which includes H2O2.
An original finding in this study is that induction of ALPCD triggers a dramatic increase in asLSU- γ RNA fragmentation, which is correlated with an extensive breakdown of rRNA and translation inhibition.
One possible explanation is that induction or maintenance of wingless expression requires Wnt6.
However, it should be noted that induction of TP53 target genes was more pronounced after SAG treatment.
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