On the other hand, p38 is phosphorylated during inflammation, cell cycle, cell death, development, cell differentiation, senescence, and tumorigenesis.
c-Jun plays an important role during multiple cellular process, including inflammation, cell cycle, and proliferation.
NF- κB is an important molecular link between chronic inflammation, cell cycle, cancer development, and cell death [ 6, 244– 244].
It is clear that statistically significant pathway maps have high relevance to inflammation, cell cycle, and cell adhesion processes.
NF-κB has hundreds of direct targets, including genes that are involved in inflammation, cell cycle and apoptosis (Perkins, 2012).
NF- κB is a family of transcription factors; RelA/p65, the main member of the canonical pathway is involved in inflammation, cell cycle progression and tumorigenesis.
MAP-kinase signaling has pleiotropic functions controlling inflammation, cell cycle, cell death, development, cell differentiation, senescence or tumorigenesis in specific cell types [ 25].
Mechanistic investigation of highly scored network nodes shows that many of them play key roles in pathways for inflammation, cell cycle, and cell adhesion – all highly associated with the pathogenesis of psoriasis.
In addition to its roles in promoting cell death and suppressing tumour formation, CYLD can also regulate diverse physiological processes including the immune response, inflammation, cell cycle progression, spermatogenesis and osteoclastogenesis.
These molecules typically inhibit translation and/or reduce the stability of mRNAs of genes involved in tumorigenic processes, such as inflammation, cell cycle regulation, stress response, differentiation, apoptosis and invasion.
