It has been proposed that modifications of the inflammatory response by caspases are central to these contrasting outcomes, and inhibit autoimmunity induced by necrotic cells.
It has been proposed that modifications in the concentration, localization, composition, or activity of RNA-binding proteins acting as splicing regulatory factors induce the splicing alterations characteristic of lung cancer [ 41].
It has been proposed that modifications of the extracellular matrix and loss of adhesion of the interdigital mesoderm to the surrounding extracellular matrix precedes the activation of intracellular apoptotic machinery.
Following this idea, a modification of popular competitive methods can be proposed that makes them self-contained.
It has been proposed that such modification serves to strengthen anticodon-codon interactions involving weaker A-U base pairs relative to those involving G-C base pairs [ 50].
Indeed, it has been proposed that posttranslational modification of H2AZ may act to regulate its distribution (Papamichos-Chronakis et al., 2011).
Hence it has been proposed that the modification of the recombinationally active length of chromosomes, either through the introduction of deletions, inversions, translocations or homoeologous sequences, can affect CO-positioning and -frequency [ 16].
In rats, it has been proposed that such modifications may lead to an alteration in the degradation efficiency of the proteasome, which could participate in sarcopenia in aging rats [ 42].
It has been proposed that epigenetic modifications of the fetal genome establish new patterns of gene expression that reset the metabolic state that is maintained into adulthood [12].
It has been proposed that combinatorial modifications at selected residues trigger specific gene expression activity [ 9].
