Oxidant exposure may trigger the post-translational modification of proteins, and nuclear transport factors are potential candidates for such modifications.
Usually, appropriate electrode surface modification may trigger reversible and multiple color states of the electrodeposition-based electrochromic device due to the absorption and/or multiple scattering of light of the modified electrode surface [30 33].
Aβ also induces DNA-PKcs carbonylation, an irreversible oxidative protein modification that may trigger its degradation by proteasomes [ 83, 84].
It would not be surprising if the production of anti-TIF1β is also linked with cancer-associated DM as overexpression and modification of self-protein may trigger an autoimmune response.
It has been suggested that certain physiologic conditions, e.g. T-cell activation [15] or mitosis [21], may trigger cytoplasmic localization of the protein, possibly via post-translational modification or modulation of RNA binding [21].
Furthermore, although the global changes more, although the global changes in histone modifications appear to be transient, with the effect peaking at about 24 hours following initial ethanol exposure, it is likely that these changes may trigger secondary changes in gene expression (including those of miRNA) or DNA modification that are much longer lasting.
Non-coding SNPs may trigger nonsense-mediated decay [31], inactivate the native splicing site [32], hinder posttranslational mRNA modifications [33].
We propose that post-translational modification of TssK or its interaction with other T6SS proteins may trigger a 'switch' between these different forms which may in turn mediate conformational changes involved in the dynamic steps of Type VI secretion.
It is possibly that activated AKT signaling may trigger downstream key transcription factors and further dynamically regulate epigenetic processes for the interplay of these two histone modifications.
Lack of employment opportunities may trigger violence and juvenile delinquency.
