The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.
|Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0||33%|
|Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0||27%|
|Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0||27%|
|Chronic Anatabine Treatment Reduces Alzheimer ’ s Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of AD v1.0.0||20%|
|In Vivo and In Vitro Characterization of Antalarmin, a Nonpeptide Corticotropin-Releasing Hormone (CRH) Receptor Antagonist: Suppression of Pituitary ACTH Release and Peripheral Inflammation v1.0.0||20%|
|Activation and regulation of the inflammasomes v1.0.0||20%|
|Discriminative Stimulus Properties of S(−)-Nicotine: “A Drug for All Seasons v1.0.0||13%|
|Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0||13%|
|Heme Curation v0.0.1-dev||13%|
Furthermore, anatabine has been recently shown to inhibit nuclear factor-kB(NF-kB) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15).
Anatabine significantly decreased the severity of EAT induced with our standard induction protocol.
Anatabine treated mice developed lower levels of thyroglobulin antibodies than controls on d 14 (P 0.029) and d 21 (P 0.045) (Fig. 2A), suggesting that anatabine atten- uates the thyroid-specific autoimmune response in- duced by thyroglobulin immunization.
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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.