Based on the prevalence of C G->T A transitions in these regions and the sequenC G->T Axtransitionstatinns, ithese been hypothesized that mutation clusteregionsander are induced by AID/APOBEC editheg deaminasequence 3].
This is in line with the previously proposed theory of Arita et al. in [ 1] and it may be hypothesized that mutations occurring in other residues located in this strand may also result in deleterious effects.
Although it has long been hypothesized that these mutations might enhance the populations of marginally-stable aggregation-prone species responsible for cellular toxicity, there has been little quantitative evidence to support this notion.
It has been hypothesized that these mutations result in a gain-of-function with respect to the elaboration of extracellular inorganic pyrophosphate.
With regard to FOXP2 and speech and language disorders, it has been hypothesized that etiological mutations in this gene affect corticostriatal and corticocerebellar networks that facilitate the learning and production of rapid movement sequences [4] and that might also be important for aspects of language function [33].
The existence of a SpeB-negative invasive phenotype has been hypothesized that results from mutations in the regulator covR/S [9].
It has therefore been hypothesized that p300 germline mutations could be associated with a disorder or phenotype other than classical RTS, which has yet to be found.
For these reasons, it has been hypothesized that when G→A mutations are ineffective in neutralizing viral genomes, the side effect is that A3G can actually promote HIV-1 diversification [ 14, 15].
It has been hypothesized that while CFH mutations and CFH/CFHR genomic rearrangements associated with aHUS impair binding of CFH to most self-surfaces, C3G-associated mutant CFHRs compete with CFH for binding to only a subset of self-surfaces, but not to endothelial cell surfaces.
These cell types are closely related and it has been hypothesized that gliomas arise by mutations in NS cells or in glial cells that have reacquired stem cell features [ 2].
