Glucocorticoids can modify cellular responses via genomic and non-genomic pathways, including regulation of ion transport processes [ 14- 17].
The insulin-signaling pathway activates a powerful gene regulator that controls many genetic pathways, including some that govern metabolism.
We identify signalogs on genomic scale in 8 signaling pathways, including the MAPK, TGF-β, and WNT pathways (for a complete list, see the Methods) from 3 intensively investigated species: C. elegans, D. melanogaster and humans, and verify their novelty and predictive power, using both bioinformatics and experimental methods.
RASSF1A inhibits the expression of the RAS oncogene, acting as a tumor suppressor gene through different pathways, including apoptosis, genomic stability and cell cycle regulation [ 41].
9, 21 Genomic profiling has shown downregulation of DNA repair pathways including BRCA1 pathway, PTEN, and TOP2A.
BRCA1 is strongly implicated in the maintenance of genomic stability by its involvement in multiple cellular pathways including DNA damage signalling, DNA repair, cell cycle regulation, protein ubiquitination, chromatin remodelling, transcriptional regulation and apoptosis.
Their proximity to genes involved in specific pathways, including neuronal development, suggests evolutionary plasticity of selected genomic regions.
USP7 also plays important roles in genomic stability by deubiquitinating and stabilizing many proteins involved in these pathways including BUB3 (Giovinazzi et al. 2014), claspin (Faustrup et al. 2009), ARF-BP1 (Khoronenkova & Dianov 2013), and others.
In contrast, the Affymetrix GeneChip, defined here as a non-targeted genomic approach, was designed to provide a survey of metabolism, spanning 27 pathways, including >300 unknown genes.
In contrast, p73 is implicated in various biological pathways including neurogenesis, inflammation, sensory pathways, and osteoblastic differentiation [18], [19] as well as genomic stability and tumor suppression [20].
In the absence of HR, these lesions prove lethal either because they persist or they can only be repaired by alternative, error-prone pathways including non-homologous end joining (NHEJ) and single-strand annealing (SSA), resulting in genomic instability.
