Evidences a(CHEBI:"amyloid-beta") to p(HGNC:BCL2L1)

Recent evidence has cogently shown that Amyloid-β induces apoptosis in rat primary neurons and human post-mitotic neuronal cells by reducing Bcl-XL expression level and evoking the release of cytochrome c from the mitochondria in a NF-κB – dependent manner

Mechanistically, the Aβ induced neuronal apoptosis has been attributed to the increase in the ratio of proapoptotic gene (BAX) transcription to that of the anti-apoptotic gene Bcl-Xl, and/or to the reduction in constitutively activated NF-κB with consequent increase in the cytoplasmic IκB proteins

In metabotrophic glutamate receptor-5 (mGlu5) agonist pretreated primary cortical neurons or neuroblastoma cells, Aβ induced toxicity was suppressed by selective activation of c-rel containing NF-κB dimers and transactivation of anti-apoptotic genes, Mn-SOD and Bcl-Xl [26] (Figs 1B, 2A)

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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.