Molecular analysis would confirm hereditary hemochromatosis, but it has a variable diagnostic sensitivity because the mutations are different in different geographic areas.
In the two species, the mutations are different, and the molecular mechanism by which less melanin is produced is different, too.
After they analyzed the mutations in different cells, both teams concluded that the tumors descended from an ancestral cancer that existed within the past few centuries.
The mutations at different positions, even distantly separated, are mutually coupled and form an evolutionary network.
We thus assessed the fitness of the mutations in different genetic backgrounds and environments.
We found that the mutations have different effects, indicative of residue-specific functions.
The mutants displayed a range of behaviours, demonstrating differential effects of the mutations at different sites in the RCL.
EPP and XLPP are clinically indistinguishable but result from the mutations of different genes: FECH and ALAS2, respectively.
The different mutations confer different levels of resistance to isoniazid.
It is found that depending on the mutation rates, different designs are evolutionarily advantageous.
