Evidences complex(GO:"NF-kappaB complex") to p(HGNC:TNF)

Another known target of NF-κB, TNFα [266, 267] is also up-regulated in the cortex [268], cerebrospinal fluid, and the serum of Alzheimer’s disease patients

Furthermore, Amyloid-β actuates NF-κB – dependent pro-inflammatory pathways in microglia culminating in TNFα expression and subsequently TNFα effectuated neurotoxicity

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients

We observed that anatabine dose dependently inhibited NFκB activation by TNFα in HEK293 NFκB luciferase reporter cells (Fig. 5) whereas nicotine was ineffective

For instance, the small GTPase Rho and its downstream effector Rho-associated coiled-coil containing protein kinase (ROCK) have been shown to contribute to TNFα induction of NFkB activation (45).

The trophic factors that evoke proliferation of NPC by inducing activation of NF-κB include epidermal growth factor (EGF) [155-161], basic fibroblast growth factor (bFGF) [155-161], vascular endothelial growth factor (VEGF) [162], tumor necrosis factor α (TNFα) [163], and erythropoietin (EPO)

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.