Sentence examples for mutations next to from inspiring English sources

It was interesting to see that all three pH-dependent Fcab mutants contained mutations next to the histidines in the EF-loop region of the parental clone.

Mutational load (Table 2, Figure 2) for a microdissected target represents the accumulation of clonally expanded LOH mutations next to tumor suppressor genes.

When LOH mutations next to these genes have been analyzed in combination with additional DNA molecular markers for genomic instability, the risk of progression increases by over 4 fold at 10 years (relative risk of 38.7) [ 33].

Baryshnikova et al (2008) were the first to investigate sputum from a large LDCT screening cohort (n=803) consisting of asymptomatic heavy smokers, assessing frequency of KRAS and p53 mutations, next to DNA promoter hypermethylation of p16, NORE1A and RASSF1A (Supplementary Table 1).

Although gene panels employed in this study and previous ones are not a complete examination of the entire genome, the absence of clonally expanded LOH mutations next to the large number of tumor suppressor genes surveyed in our panel is strong evidence that the microdissected targets examined did not have extensive genomic instability.

Moreover, in P2 there was another mutation next to the second histidine.

Strikingly, all three pH-dependent Fcab mutants contained a mutation next to the histidine located at the last position of the randomized EF-loop region (Table 1).

Only the LM-G41R seems to be N-terminal cleaved upon mitochondrial import [ 38, 73], possibly because of the enhanced conformational fluctuations caused by the mutation next to the MTS [ 43], which suggests that the MTS is not generally cleaved upon import of hAGT as observed for many other MTS-containing proteins.

This mutation lies next to the K531 residue (shown in purple in Fig. 7a) that has been shown to confer heparin binding to wild-type AAV6 [35].

KEAP1 mutations are found, next to abnormally increased DNA methylation, to impair KEAP1 function, thus liberating NRF2 to the nucleus.

ALK mutations V1149L and A1266T are located next to previously described mutations L1152R 37 and G1269A 38, which have been identified as resistance mutations to Crizotinib and other tyrosine kinase inhibitors, and could then have the same impact on treatment response.