The molecular basis of hybridization-induced element derepression is not fully understood but likely involves disruption of one or more host repression systems as a consequence of merging differentiated genomes.
Hybridization has been demonstrated to activate LTR retrotransposons in several species groups (Waugh O'Neill et al. 1998; Labrador et al. 1999; Liu and Wendel 2000), presumably due to the disruption of host repression mechanisms as a consequence of merging differentiated genomes.
Patients with negative MIBG studies were found not to express vesicular monoamine transporter expression (VMAT-1) likely as a consequence of the poorly differentiated nature of these tumours.
This differential reactivity might be a consequence of a particular and differentiated exposure of each one of the antigens to the host immune system due to their specific location in the parasite [ 27, 34] or, alternatively, to the ability of the immune system to recognize antigens depending on the stage of the illness.
These phylogenetic relationships can be interpreted either as a consequence of old hybridization among differentiated lineages [ 21] or as a result of much more recent human-mediated translocations [ 25].
16S analysis commonly provides a definitive identification, but certain closely related species cannot be differentiated, a consequence of the low level of interspecies polymorphism and the existence of multiple and different copies of 16S in N. nova [11, 2].
The three neurofilament genes (NF-L, NF-M, NF-H) were differentially expressed in the undifferentiated and differentiated conditions, possibly as a consequence of being independent transcription units and hence were differentially regulated [26].
Results indicate that MRP mRNA levels in a greater proportion of high-grade (G3) bladder tumours (55%, 6/11) are significantly reduced (P=0.018) compared with low- and moderate-grade (G1/2) bladder tumours (8%, 1/13), and suggest that MRP mRNA levels frequently become reduced as a consequence of tumour progression to advanced, poorly differentiated disease.
The presence of colonies composed entirely of neurons, or containing no neurons (Figure 1B, C) suggests that the eventual phenotype of the differentiated cells is a consequence of a lineage decision made at the point of induction to differentiate.
After in vitro exposure to Infliximab, there was a lack of effector cells, suggesting that this drug might block the lineage pattern of differentiation (naive → memory → effector → terminally differentiated cells), as a consequence of expansion and activation inhibition.
