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Schep LJ et al (2009): Nicotinic plant poisoning

Current data emphasizes receptor selectivity, intracellular pathways, and broader systemic observations, but no definitive applications have been established

These findings identify a novel mechanism for ACs anticancer effects in glioblastoma, highlighting its potential as a therapeutic agent by suppressing EMT and tumor aggressiveness through ubiquitin-mediated degradation of c-Met (Hei et al

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LONP1 regulates mitochondrial accumulations of HMGB1 and Caspase-3 in CA1 and PV neurons following status epilepticus