Similarly, the burden of all functional categories is ordered by common expectations as to how often such mutations are expected to be functional.
FHM2 mutations predict reduced glial uptake of K+ and glutamate from the synaptic cleft whereas FHM3 mutations are expected to be associated with hyperexcitability of excitatory neurons.
Partly, this reflects the fact that the mitochondrial gene products are essential for life; that is, most mtDNA mutations are expected to be lethal.
The structural consequences of the two mutations are expected to be distinct [20].
These mutations are expected to be selected by AZT, and perhaps by other NRTI, particularly thymidine analogues.
Since true adaptive mutations are expected to be present in both lineages, we analyzed each lineage separately, discarding sites that are not shared by both human influenza lineages.
Random mutations are expected to occur more frequently in nucleotide positions that are not relevant for molecular functions and in genes not necessary to express a differentiated phenotype.
In small populations (e.g. in endemic island species), the dynamics of non-synonymous mutations is dominated by drift and the fixation probabilities of deleterious and advantageous mutations are expected to be approximately equal [5].
While protein kinases have a prominent role in tumorigenesis, commonly mutated protein kinases in cancer appeared to be the exception to the rule and most of kinase driver mutations are expected to be distributed across many protein kinase genes [27].
Zheng has previously noted that classic estimates of the probability of the occurrence of double mutants ignore the fact that sequential random mutations are expected in a growing population of bacteria[14].
These mutations are expected to abolish DNA binding.
