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We then used ABA1 to screen for aptamers that can form binding pairs using the aptamer array.
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For the evaluation of the model we also include a performance evaluation for the classification of drug target pairs into binding or non-binding, using the metrics AUC and AUPR.
Second, we made within-pair comparisons to test the significance of intra-pair differences in SERT binding in twin pairs discordant for BN and in healthy twin pairs by using the paired nonparametric Wilcoxon test.
To correlate ABS accessibility and sequence with efficiency of RNA duplex formation we determined the binding affinity for the mRNA/gRNA pairs using EMSA, as previously described [13].
To extract the functional TF-gene binding pairs, we used a network approach to combine the ChIP-chip data and the TFKO data.
Specific binding for each pair of sections used for receptor studies was calculated by subtraction of the mean nonspecific binding from the mean total binding using the whole sections as the region of interest.
Briefly, this approach calculated a binding probability score for each TF-gene pair using all the evolutionarily conserved TF binding sites (TFBS) in proximal promoters and evaluated a P-value using TFBS permutation (see Methods, Additional file 8: Figure S1).
The second one, called the TF-gene binding network, was constructed using the TF-gene binding pairs.
The metal binding capability was evaluated using the binding energy.
However, as was described in Brooks et al. [ 44], it is possible to dock the PK kinase domain pairs in trans using the binding surfaces proposed by earlier studies which locate the key V617F PK mutation close to the activation loop of the kinase domain [ 75– 75].
A fragment of 488 bp of N gene of PPRV containing the real time RT-PCR primers binding sites were amplified using the primer pair N3F (forward primer): 5′-CAAAGC GCCGA CGGCA TCA GGTT-3′ (48 70) and N3R (reverse primer): 5-′GCCAGAAGGATCCAGACTTGTGC-3′ (514–536) (In house designed).
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