Overexpression of amyloid precursor protein is associated with degeneration, decreased viability, and increased damage caused by neurotoxins (prostaglandins A1 and E2, hydrogen peroxide, and nitric oxide) in differentiated neuroblastoma cells.
D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis* / Q000235:genetics*; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D015232:Dinoprostone / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation / Q000502:physiology; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D051379:Mice; D009410:Nerve Degeneration / Q000235:genetics* / Q000473:pathology*; D009447:Neuroblastoma / Q000235:genetics* / Q000473:pathology*; D009498:Neurotoxins / Q000633:toxicity*; D009569:Nitric Oxide / Q000633:toxicity; D011454:Prostaglandins A / Q000633:toxicity; D014407:Tumor Cells, Cultured
D016564:Amyloid beta-Protein Precursor; D009498:Neurotoxins; D011454:Prostaglandins A; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D015232:Dinoprostone; C100573:prostaglandin A1