a(CHEBI:nicotine) decreases bp(GO:"apoptotic process")

View Subject View Object

PubMed:19293145

Nicotine protects PC12 cells from cell death resulting from serum depletion through a mechanism that depends upon the function of IP3 receptors, L-type calcium channels, ryanodine receptors, and ERK, suggesting that the protective effect of nicotine is mediated by calcium signaling pathways (Ren et al., 2005).

Related Edges 8

• a(CHEBI:nicotine) association bp(GO:"calcium-mediated signaling")
• a(CHEBI:nicotine) association p(HGNCGENEFAMILY:"Inositol 1,4,5-triphosphate receptors")
• a(CHEBI:nicotine) association p(HGNCGENEFAMILY:"Ryanodine receptors")
• a(CHEBI:nicotine) association p(FPLX:ERK)
• bp(GO:"calcium-mediated signaling") association a(CHEBI:nicotine)
• p(FPLX:ERK) association a(CHEBI:nicotine)
• p(HGNCGENEFAMILY:"Inositol 1,4,5-triphosphate receptors") association a(CHEBI:nicotine)
• p(HGNCGENEFAMILY:"Ryanodine receptors") association a(CHEBI:nicotine)

Experimental Factor Ontology (EFO)

PC12

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.

---