a(CHEBI:nicotine) decreases tloc(p(HGNC:BAX), fromLoc(GO:cytosol), toLoc(GO:mitochondrion))

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PubMed:19293145

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005).

Related Edges 6

• a(CHEBI:donepezil) increases p(HGNC:BCL2)
• a(CHEBI:galanthamine) increases p(HGNC:BCL2)
• a(CHEBI:nicotine) increases p(HGNC:BAX, pmod(Ph))
• a(CHEBI:nicotine) decreases bp(GO:"apoptotic process")
• a(CHEBI:tacrine) increases p(HGNC:BCL2)
• tloc(p(HGNC:BAX), fromLoc(GO:cytosol), toLoc(GO:mitochondrion)) increases bp(GO:"apoptotic process")

MeSH

Neurons

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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.

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