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CNA is only one factor that could be driving pathway involvement in phenotypes.
One pathway preferentially targeted through large terminals CB+ thalamic neurons enriched with ionotropic glutamate receptors at the synapse, consistent with a driving pathway.
This enhanced expression of ligands is likely the primary force driving pathway activation, and is manifested in dramatically increased expression levels of many pro-inflammatory chemokines.
Another pathway originated preferentially from PV+ thalamic neurons and targeted preferentially the middle layers of prefrontal cortex, through generally larger terminals, consistent with a driving pathway.
Calbindin thalamic neurons, in turn, were innervated by prefrontal axons through small and large terminals that formed asymmetric synapses preferentially at sites with ionotropic glutamate receptors, consistent with a driving pathway.
On the other hand, the thalamo-cortical pathway that terminates in the superficial layers is thought to be modulatory, and the cortico-thalamic pathway from layer V appears to be a driving pathway [11], [18] [21].
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The activation of the PI3K/Akt cell survival pathway through alternate RTKs may protect against TGF-β induced apoptosis while driving pathways critical to carcinogenesis.
Heterogeneity in driving pathways and in the phenotypes of T-ISC has become increasingly apparent (Patel et al, 2012; Schober & Fuchs, 2011; Visvader & Lindeman, 2012).
A rigorous approach would be to integrate cell-cycle driving pathways into the model, as was done to investigate the interplay between cell cycle and DNA-damage response pathways regulating cell cycle arrest.
In this study, we sought to gain a comprehensive understanding of the key driving pathways for osteosarcoma by performing pathway analysis of recurring gene copy number aberrations using array comparative genomic hybridization (aCGH) analysis.
Although many enzymes driving this pathway have been identified, regulatory mechanisms underlying this system remain elusive.
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