Bet v 1l crystallized as a monomer [18] probably because N28K mutation could prevent the formation of Bet v 1 like dimer.
If a gene contains mutations that could prevent correct expression (i.e. missing start codon or stop codon, non canonical splicing site, frameshift or in frame stop codon), it was considered as a pseudogene.
By regulating the synthesis of alternatively spliced isoforms skipping the nonsense mutation, NAS could prevent the production of deleterious truncated proteins [38] [43].
Markers with low mutation rates could prevent or reduce the probability of detecting population differentiation, even in truly non-panmictic populations [ 5].
Thus we raised the hypothesis that wild-type ΔNp63 α could be acetylated by p300 on K193, and that mutations of this residue could prevent this post-translational modification with important developmental consequences.
It is possible that severe mutations in TTP coding sequences could prevent or decrease the expression of mature transcripts, interfere with splicing of the single intron, or lead to frame-shift or stop-codon mutations.
For some diseases, correcting the mutation in even half of the affected cells could prevent symptoms and essentially cure the disease.
Moreover, Ward et al. also showed that mutations in a dileucine motif of a chimeric B5 protein could prevent plasma membrane retrieval, as measured by antibody uptake and staining, implying a mechanism for B5 retrograde trafficking [87].
We have genetically tested whether enhanced lens gap junction communication, provided by increased α3 connexin (Cx46) proteins expressed from α8(Kiα3) knocknock-ineles in Gja8tm1(Gja3)Tww mice, could prevent nuclear cataracts caused by the γB-crystallin S11R mutation in CrygbS11R/S11R mice.
This could prevent rare alleles from being lost from the population, increasing the ability of mutation and migration to maintain recognition locus diversity [ 17].
