ESR1 mutations appear to drive oestrogen-regulated processes in resistant tumours.
These mutations appear to be tremendously important, yet neither Mendelian nor GWAS techniques can detect them.
This approach is made tractable by the finding that stability-enhancing mutations appear to be relatively common in membrane proteins.
In particular, GBA and LRRK2 mutations appear to be considerably frequent in our population, suggesting a strong Jewish influence.
Rohner and Aspiras found that the mutations appear to reduce the gene's activity in the cavefish, taking the brakes off their appetite suppressor.
Some of the mutations appear to be common, while some rare variants seem to cause the same symptoms as those experienced by individuals with a completely different set of rare mutations.
Thus, LTM mutations appear to influence the frequency of LFP oscillations in the fly brain as well as visual behavior.
Remarkably, we also found that 13 out of the 24 mutations appear to be fast-acting, making them particularly useful for careful dissection of multiple essential requirements.
This is consistent with the SWISS-PROT mutagenesis dataset, in which only 3.4% of mutations appear to be gain of function mutations.
Thus, enz mutations appear to result in similar reductions in the numbers of differentiated chromatophores, while other neural crest-derived cell types are unaffected.
The lon promoter mutations appear to arise readily by spontaneous transposition of IS186 to a single site, and in either orientation [14].
