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Similarly, a mutation can generate a cheater with respect to this site, with lower expression.
However, the fact that the JAK2+ syndromes exhibit various clinical features raises the question of how a single mutation can generate different MPNs and strongly suggests that other acquired events have to occur, at least in ET and PMF.
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Cancer somatic mutations can generate neoantigens that distinguish malignant from normal cells.
These mutations can generate both aberrant and correct transcripts, the level of which varies among different patients.
But the mutations can generate an incredible number of effects on the phenotype, and most of them will be deleterious under any circumstances, if not lethal.
These compensatory mutations can generate variants with high transmission fitness (δrH), comparable to that of the wild-type strain.
Using this method, we show here that MCU does recapitulate key features of I MiCa, and show that a single point-mutation can generate resistance to pharmacologic inhibition.
Genetic diseases caused by nonsense or frameshift mutations can generate premature termination codons, which usually trigger nonsense-mediated mRNA decay (NMD).
Uniquely, ENU-induced mutations can generate not only null alleles but also partial loss-of-function (hypomorphic) and dominant-negative alleles (Acevedo-Arozena et al., 2008).
Note that some nonsense and frameshifting mutations may not generate null alleles if they only disrupt a short C-terminal region of the encoded protein, whereas some missense mutations can generate null alleles.
We propose that the exclusive identification of spliceosome gene mutations in those aged ≥70 years can be explained by differences in the prevailing pressures on clonal selection at different ages, which can in turn explain how different gene mutations can generate detectable clonal expansions at different ages.
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