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To examine how the structure got damaged and leads to affect the functions upon mutation, we analysed the native and mutant (R326H and R356Q) structures at different time scales.
To investigate the potential role of any selection on synonymous sites in the disparity between dS and other measures of mutation, we analysed the rates of divergence observed across intron-exon boundaries [ 18].
To assess the co-occurrence of the two BRCAness measures and BRCA1 mutation, we analysed the neoadjuvant series, as this series was the most complete for the three data types and not biased towards familial cases.
In order to understand the structural consequences of the VH-71Arg → Ala mutation, we analysed the impact of this mutation on the conformation and relative position of antigen-binding loops (CDR-H1 and CDR-H2) and calculated the buried surface area of the interface between the two motifs CDR-H1 and CDR-H2 for the three huHMFG1 models.
In the current study, in order to better elucidate the clinical characteristics of the V180I mutation, we analysed the surveillance data of 186 patients with V180I, including the occurrence rate of neurological symptoms, the period of time between disease onset and the occurrence of these symptoms, biomarkers in the CSF, MRI and EEG data, and codon 129 polymorphism in PRNP.
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As our findings in NSCLC cell lines suggested concurrency of KRAS or BRAF and mutual exclusiveness of EGFR mutations with LKB1 mutations, we analysed the mutational status of these genes in our primary NSCLC tumour specimens.
As the T242N mutation has been previously linked with compensatory mutations we analysed our cohort to see if these accrued in late stage disease to explain the rise in viral fitness despite the maintenance of T242N.
Of the 194 single bp mutations we analysed from Wormbase (Additional File 1) 50% resulted in missense alleles and the remaining 50% in nonsense or splice junction mutations.
To estimate the importance of the DNE of TP53 mutations, we analysed the percentage of cancer cases showing a single heterozygous mutation of TP53 and searched for a cell line with a single heterozygous mutation of this gene.
To screen for B-RAF mutations, we analysed DNA extracted from paraffin-embedded tumour tissue and adjacent thyroid tissue of patients who presented GRIM-19 mutations following the procedures previously described (Davies et al, 2002; Soares et al, 2003).
Since the patient is heterozygous for the K16N mutation we also analysed the equimolar mixtures of both peptides (Aβ mix).
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