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Too many preclinical candidates in a given time-frame could potentially stress development resources and thereby increase downstream cycle times.
During the downstream cycle, the sound wave travels with the flow of blood, which results in a decrease in total transit time for the same flow amount.
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The fluxes in EMP and in downstream TCA cycle were 50 and 67% higher on Glc/Glu than on Glc, respectively.
The fluxes in EMP entry reaction and in downstream TCA cycle were 50 and 67% higher on Glc/Glu than on Glc, respectively.
The net generation rate of NADH was about 25% higher on Glc/Glu than on Glc (2.72 vs. 2.18 μmol/gDCW/s) correlating with the higher fluxes in downstream TCA cycle.
We could then time downstream cell cycle events relative to the external clock and thereby better isolate the sources of variability.
The proliferative effects of Shh are likely mediated through the transcriptional regulation of Shh target genes that include several transcription factors (e.g. NMyc) [15] and downstream cell cycle regulatory proteins (e.g. CyclinD1) [16].
Further analysis of the downstream cell cycle modulators known to be influenced by Akt signalling was also undertaken.
Tel1p then functions to phosphorylate its targets both within this complex and downstream cell cycle targets such as p53.
In parallel, flux through glycolysis and the downstream TCA cycle serves to sustain energy levels required for gene expression and anabolic reactions during ripening.
Thus, the effects of PDCD2 loss appear to involve induction of p53 and the p53 direct target gene, p21, with reduction of downstream, cell cycle promoting genes.
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