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With this cut-off all but one mutation were analyzed correctly (98.6% sensitivity).
Allelic expression imbalance (AEI) and cDNA mutation were analyzed in 13 pairwise lesional tissues (LTs) and neighboring normal-appearing skin (NNS) to investigate the underlying pathogenicity of PK.
In the Steagall et al. (2007) [ 19] study homozygous patients with the delF508 mutation were analyzed for their reactions to Bronchodilation.
For each mutant line, F2 progenies that contained the SRKb- SCRb transgenes and were homozygous for the insertional mutation were analyzed by pollination assays of stigmas at the −1 bud stage.
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To further analyze p19-RACK1 intheaction, the C-terminal of p19 was mutated at three positions, S160A, W164A, and D165G, and each single mutation was analyzed by yeast two-hybrid assays.
TP53 mutation was analyzed by Sanger sequencing in 396 tumors: 64/178 (35.9%) IDH mutated tumors were also mutated on TP53, versus 49/218 (22.5%) of the nonmutated tumors (P = 0.0036).
HFE mutation was analyzed measuring fragment-length polymorphisms by PCR [1].
249Ser mutation was analyzed by RFLP and DNA sequencing.
DNA from 376 pagetic patients and 297 controls, all without any SQSTM1/P392L germinal mutation, was analyzed.
The mutation was analyzed in the whole family and showed full co-segregation with the phenotype.
When the M59I mutation was analyzed within the pseudotyped particle entry assay, a similar resistance phenotype was observed.
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