act(a(CHEBI:"glutamate(2-)")) increases bp(HBP:Excitotoxicity)

View Subject View Object

PubMed:19293145

Nicotinic neuroprotection against non-Abeta toxicity is also mediated largely through alpha7 nAChRs. alpha7 nAChRs protect PC12 cells against ethanol toxicity (Li et al., 1999a) and from cell death associated with serum depletion (Ren et al., 2005); they protect cultured neurons against glutamate-induced excitotoxicity (Kaneko et al., 1997) and hippocampal slices against oxygen and glucose deprivation (Egea et al., 2007) through the activation of alpha7 nAChRs (Rosa et al., 2006).

Related Edges 7

• act(a(CHEBI:ethanol)) increases path(HBP:neurotoxicity)
• a(MESH:Serum) decreases bp(GO:"cell death")
• act(p(HGNC:CHRNA7)) decreases act(a(CHEBI:ethanol))
• act(p(HGNC:CHRNA7)) decreases bp(GO:"cell death")
• act(p(HGNC:CHRNA7)) decreases act(a(CHEBI:"glutamate(2-)"))
• act(p(HGNC:CHRNA7)) increases a(CHEBI:glucose)
• act(p(HGNC:CHRNA7)) increases a(MESH:Oxygen)

MeSH

Neurons

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.

---