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A combination of various mutations has often a cumulative effect on the thermostability of family 11 xylanases.
Detection of KRAS mutations has often been the primary validation for many of the numerous polymerase chain reaction (PCR) based mutation detection methods.
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Studies on the molecular consequences of such mutations have often been conducted in bacterial models of complex I [58 61].
This type of directed carrier testing is relatively straightforward because there is a known history of the disorder and because the causative mutation has often been identified in the proband.
Single-point mutation analysis has often resulted in perplexing results, which are difficult to simulate using computation.
Indeed, Vogelstein et al. (2013) recently noted that the best way to identify driver genes is not through their mutation frequency as has often been done in the past, but rather through their spatial patterns of mutation.
However, emergence of pathogenic revertants from live attenuated SIVs by spontaneous mutations as well as by recombination has often been encountered in macaque AIDS models [23] [28] and certainly during our study.
Selection has often been toward loss-of-function mutations.
In addition, TP53 protein accumulation has often been used as an indirect indicator of mutation.
Influenza represents a particularly problematic therapeutic challenge since high viral mutation rates have often confounded many conventional antivirals.
TARDBP and FUS mutations have most often been associated with a classical ALS phenotype.
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