Hence, we hypothesize that instead of mutations in tubulin, a post-translational modification that would affect its polymerization status as is affected by the E3 ligase, MGRN1, would similarly alter α-tubulin monomers and affect α-tubulin functions at the cellular as well as the organismal levels.
However, the imp-β KetRE34 deleterious effect could not be directly attributed to Imp-α2 but to modifications occurring in Imp-β that would affect the binding of factors to Imp-α2.
The question is whether that would affect learning.
To our knowledge, even in cancer, where recurrent somatic mutations in hot spots are well known (e.g., mutation V600E in BRAF or mutations in codons 12 and 13 of KRAS in colorectal cancer) [Oliveira et al., 2007], a triple nucleotidic modification that would systematically affect three distinct and nonadjacent codons has never been described.
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Ngn2 is also known to oscillate in progenitors (Shimojo et al., 2008), and although it is not subject of the same type of negative feedback loop as Hes1, it is quite possible that posttranslational modifications would affect its oscillatory properties, potentially due to changes in protein stability.
We hypothesized that the design modifications would affect postoperative clinical outcomes and complications after TKA.
Due to the purpose of the embryo transfer was to make transgenic animals, there is possibility that the different genetic modifications would affect the cloning efficiency.
A second caveat is that the RT-qPCR method used in this study would not account for post-translational modifications that may affect secretion, function or half-life of the antimicrobial peptides.
