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In addition to point mutations, other mutations were generally shown as the changes in genomic structure: inversion, transposition, translocation and duplication, gene gain and gene lost, gene fusion and gene split, gene fragmentation (pseudogene) or insertion and deletion (indel).
The multi-alignment analysis of the 59 pseudogenes demonstrated that the mutations were generally resulted from frameshift: except 4 genes interrupted by ISHp609 and 4 gene with the occurrence of new stop codon by point mutations, 60 premature mutations were formed by frameshifts (Figure 7a, Table S3).
In contrast, singleton mutations were generally of lower abundance but large in number.
For genotype analysis, mutations were generally categorized according to the International AIDS Society-USA recommendations [ 17].
Fourth, mutations were generally of the same type for long genomic distances and then could switch to a different class.
These mutations were generally found to be IS 6110 strain lineage-specific, although examples of additional within-lineage and even within-cluster mutations were observed.
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One of these approaches is based on pathogenic mtDNA mutations being generally heteroplasmic, with observable pathology only present when the ratio of mutated mtDNA exceeds a certain threshold.
Also, it has to be emphasized that current large screening initiatives based on primary airway cells are not able to target rare CF mutations, since explanted lung tissue homozygous for rare mutations is generally not available.
The many available crystal structures of RT reveal that, generally, in relation to their binding sites NRTI resistance mutations are generally more distally positioned, whilst for NNRTIs mutations are clustered.
ATR-X patient mutations are generally hypomorphic and do not cause chromosomal instability[4].
However, microdissection and sequencing of breast cancer samples suggest that p53 mutations are generally, if not virtually always, clonal within breast cancer [30], [31].
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