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NADPH regeneration rates from genome-integrated pathways were estimated using a NADPH-binding fluorescent reporter and by the productivity of a NADPH-dependent terpenoid biosynthesis pathway.
The P values describing the statistical significance of the overrepresentation of GO terms in the pathways were estimated with (two-tailed) Fisher's exact tests and corrected to account for multiple-hypotheses testing using the Benjamini & Hochberg adjustment procedure [7].
In addition, 90% of targets from canonical pathways were estimated to be expressed.
The simple enriched pathways were estimated by the DAVID program [ 30] in which the p values of each pathway were calculated, based on Fisher's exact test, from an input list of genes.
Legal import pathways were estimated by using stochastic quantitative models; consequently, an absolute probability of the risk of ASFV entry was obtained per country (available in Additional file 1).
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The metabolic efficiency of these pathways was estimated by calculating intrinsic clearance (Vmax/Km).
Accordingly, the mammalian MAPK pathways are estimated to be deregulated in one-third of all human cancers [ 149].
The degree of association of the five metabolic pathways was estimated by calculating their odds ratios (ORs) using conditional logistic regression analysis.
Specifically, the interaction score between two pathways is estimated by their overlapping status of weighted pathways in the following formula: The overlapping score is the summation of the scores of overlapping edges between pathways.
To check whether they were involved in the increased resistance of DN-AtRop1 transgenic lines to P. infestans, the transcript level of marker genes in these two pathways was estimated by RT-PCR.
The risk of entry via legal import pathways was estimated by quantitative models, whereas risk was assessed by semi-quantitative models for illegal imports, wild boar and transport-associated fomites.
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