Title : Smoking exposure induces human lung endothelial cell adaptation to apoptotic stress.

Pub. Date : 2014 Mar

PMID : 24079644






3 Functional Relationships(s)
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1 In these cells, caspase-3 was inhibited by ceramide-induced Akt phosphorylation, and by the induction of autophagic microtubule-associated protein-1 light-chain 3 lipidation. Ceramides AKT serine/threonine kinase 1 Homo sapiens
2 In cells from smokers, the prominent up-regulation of Akt pathways inhibited ceramide-triggered apoptosis, and was associated with elevated sphingosine and high-mobility group box 1, skewing the cell"s response toward autophagy and survival. Ceramides AKT serine/threonine kinase 1 Homo sapiens
3 In conclusion, the cell responses to ceramide are modulated by an intricate cross-talk between Akt signaling and sphingolipid metabolites, and profoundly modified by previous cigarette smoke exposure, which selects for an apoptosis-resistant phenotype. Ceramides AKT serine/threonine kinase 1 Homo sapiens