Sentence examples for deleterious frame from inspiring English sources

Deleterious frame shift mutation, c.3086delT in exon 11 was identified in one patient who developed breast cancer at the age of 46 years.

Under the hypothesis that the SSTI isolates are evolving away from a virulent phenotype we looked for an enrichment of genes harboring unique nonsense, ns-cSNVs or deleterious frame shift mutations among the SSTI isolates in genes related to virulence.

We observed more indels of three or six bases (Additional file 6: Figure S6B), probably due to the negative selection of sizes not equal to multiples of three bases in coding sequences because they cause deleterious frame shift mutations.

Two novel deleterious frame-shift mutations; c.3086delT/exon11 (in one patient) and c.5404delG/exon21 (in one patient and two of her family members) were identified.

In contrast, if the under-representation would be a consequence of selection against targets of deleterious frame-shift mutations, one would expect selection to act much less efficiently towards eliminating trinucleotide repeats, because changes in them do not lead to a frame-shift.

Two novel deleterious frame-shift mutations, c.3086delT in exon 11 [BIC: AC:17840] and c.5404delG in exon 21 [BIC: 17841], and one novel missense possibly pathogenic mutation, c.856T>G in exon 11 [BIC: AC17839] were detected (Table 2).

The long-term effect is difficult to fully characterize, because the SSR is only a pre-deleterious allele and its impact on fitness will be only moderate unless the deleterious frame-shifted allele is extremely likely to appear and is associated with a strong impact on fitness.

No homozygous deleterious mutation (frame-shifts, in-frame insertions or deletions, stop gain or loss of variants as well as polymorphisms that affect splice donor or splice acceptor sites and missense polymorphisms predicted to be deleterious) was found with this approach.

The rate of inactivating mutations of TAAR sequences under neutral evolution was determined by counting all pseudogenization events in branches in which the respective TAAR is already inactivated by deleterious mutations (frame-shifting indels, stop codons) in its ancestral branch assuming the primate phylogeny as stated above.

Combination of such physical interaction data (at least two interaction partners) and deleterious in-frame mutations (at least one) for proteins helped us to identify proteins those are subject to edgetic perturbations (Zhong et al. 2009).

This prediction is based on the possibility of a variant to be e.g. deleterious or in-frame.