Sentence examples for mutation analyses indicated from inspiring English sources
VEGF promoter deletion and point mutation analyses indicated that a region between nucleotide -109 and -61 and its intact Sp1-binding sites were required for the inhibition of VEGF promoter activity by celecoxib.
Further deletion and point mutation analyses indicated that mutation of individual or all of the putative Sp1 binding sites reduced or eliminated the constitutive VEGF promoter activity and abrogated the differential activity of the promoter in high and low VEGF-expressing cells.
Previous mutation analyses indicated that most pathogenic substitutions in CAPN3 either influence its activity directly or indirectly by modifying its autolytic properties.
This tendency was also observed in the present study, but mutation analyses indicated that hot spot mutations were not detected in the mucosal part of the tumours, except in 1 intramucosal cancer (#M12).
This residue is in the convex surface of the protein, opposite to the one supposed to bind SNARE complexes; however, mutation analyses indicate that this area is also important for αSNAP function [27].
In vivo and in vitro analyses indicated that mutations Cys69Ala and/or Cys96Ala have a minor impact on NblR function, structure, size, or oligomerization state of the protein, and that Cys69 and Cys96 do not seem to form disulphide bridges.
Further analyses indicated that this mutation arose relatively recently in equine evolution and was spread by horse breeders.
Model-based analyses indicated that Y992F mutation caused rapid EGFR degradation through the up-regulation of EGFR ubiquitination and aberrant temporal activation of ERK1 by network-wide activation of tyrosine-phosphorylation; this suggests that pY992 strengthens and attenuates phosphotyrosine singling by distinct regulatory mechanisms.
As shown in Table 2, multivariate logistic regression analyses indicated that ESR1 mutation-positive breast cancer cases were more likely to have ever used OCs (OR = 1.72, 95% CI = 0.66 to 4.44), but this result was not statistically significant.
Gene-ontology analyses indicated that the F170I mutation altered the expression of genes involved in oncogenic pathways.
Although the bioinformatic analyses indicated all four ZC4H2 mutations were likely pathogenic (Table 2), we undertook in silico analyses to predict the effect the three missense mutations had on the stability of the ZC4H2 protein.
