The most common types of mutation are attributed to small insertion/deletion frameshift, nonsynonymous truncation, and disruption of splice site leading to entire nonfunctional BRCA proteins.
Some of the variation is attributed to specific mutations in PSEN1 [ 54– 54].
For inhibitors characterized by slow dissociation rates to wild-type enzyme (saquinavir and nelfinavir), the decrease of affinity conferred by additional mutations was attributed to increased koff values.
Progeny cells are assumed to have identical genomes, in the case of which mutations are attributed to WGA artifacts.
During SHM, 73% of the mutations are attributed to AID and error-prone polymerase eta (POLη).
Specifically, Arg mutations were attributed to the anti-viral immunity and cell cycles of APOBEC3G [ 50, 51], which is consistent with previous mutational signature analysis study [ 49].
The activation of silent genes by the rpoB H437D or H437L mutations was attributed, at least in part, to the increased affinity of mutant RNAP for the silent gene promoters (Hosaka et al. 2009).
The universality of this mutation spectrum is attributed to its underlying mechanism, namely transcription-coupled DNA repair [3,4].
As the divergence between D. melanogaster and D. simulans does not follow this pattern, the drop in variability cannot be explained by mutation rate variation, but is attributed to selection [27], [28].
Although the human disease associated with mutations in GUCA1A is attributed to gain-of-function mutations and the knock-out mice have no discernible retinal degeneration, this study has advanced our understanding of the regulation of guanylate cyclase activity by GCAP proteins.
