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In studying the phenotype of the kto/med12 mutation we focused our attention on the hindbrain in the zebrafish embryo.
For the identification of pathways significantly affected by the mutation, we focused on the metabolite pathways with at least three affiliated genes.
And for the identification of pathways significantly affected by the mutation, we focused on the metabolite pathways at least 3 genes affiliated.
To determine whether these evidence apply to the particular case of the Gly251Ser mutation, we focused on the loop that harbors the target residue 251.
For the binding mutation, we focused on the largest of the three surface loops (residues 79 90 in FN3-HA4) whichwhich FN3 monobodies contact their targets.
Similar(55)
Given the absence of high resolution crystal structures of kinase cancer mutants and nature of large conformational changes caused by activating mutations, we focused on understanding local functional effects of cancer mutations rather than attempting to make computational predictions of the mutant structures.
Among these 7 mutations, we focused on the Il4ra p.S540frameshiftift mutation.
In addition to nonsense and frameshift mutations, we focused on dysfunctional mutations predicted to be deleterious by SIFT or PolyPhen-2 programs.
Among the remaining mutations, we focused on those located in the genes encoding DNA repair-related proteins and identified a novel mutation of RNF8.
In order to go further in the identification of alterations linked to EGFR mutations we focused on genes implicated in cell cycle regulation and validated SNP array information on a large series of NSCLC.
To test for phenotypic consequences of predicted functional mutations, we focused on nonsynonymous SNPs in genes encoding transcriptional regulators in Lineages 1 and 2. We identified 11 genes with lineage-specific SNPs predicted by SIFT analysis as likely to impair protein function and a further three genes with nonsense or frameshift insertion/deletion (indel) mutations (table 2).
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