Sentence examples for mutations were assessed from inspiring English sources

Alternate approaches for correcting the majority of X-CGD mutations were assessed, involving TALEN- or Cas9-mediated insertion of CYBB minigenes at exon 1 or 2 of the CYBB locus.

The correlations of the in vitro response to AZD6244 or MK2206 (IC50) and gene mutations were assessed by using Wilcoxon test and Logistic regression.

However, some of these proteins contained multiple TRD mutations, were assessed only for a limited number of phenotypes, or were evaluated in different cell types that complicated or precluded cross-study comparisons [10], [14], [15], [28].

Differences in persistence of NVP-R mutations were assessed in a small number of infants exposed to SWEN (n = 5) or SD-NVP (n = 5) who had available plasma samples and also had NVP-R mutations detected by standard population sequencing at the time of HIV diagnosis (Table 4).

Locations of mutations were assessed using the CEN.PK consensus sequence as a guide.

TP53 mutations were assessed by denaturing gradient gel electrophoresis analysis and DNA sequencing.

The effect of the mutations was assessed by circular dichroism spectroscopy from urea-induced equilibrium unfolding experiments and in time-resolved mode to follow the kinetics of refolding and unfolding.

To test this hypothesis, mutations were introduced at each of the three sites, and the effect of mutations was assessed using CAT-based transient expression assay.

Amino acid conservation at the missense mutations was assessed using SIFT software (http://sift.jcvi.org/) and Polyphen was used to predict the effect of the variation on the protein (http://coot.embl.de/PolyPhen/).

The disease burden of all the mutations was assessed by the CMT Neuropathy Score (CMTNS) and CMT Examination Score CMTESS).

The sequence context of MMC-induced mutations was assessed by extracting the 15 flanking nucleotides around the deletions for analysis.