Na/Ca exchanger overexpression induces endoplasmic reticulum stress, caspase-12 release, and apoptosis.
This paper describes a possible strategy to control Ca(2+) homeostatsis as a possible approach to prevent or enhance beta-cell apoptosis
Díaz-Horta
Oscar
O
Laboratory of Pharmacology, Brussels University School of Medicine, Brussels, Belgium.
Van Eylen
Françoise
F
Herchuelz
André
A
D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D053454:Caspase 12; D020169:Caspases / Q000378:metabolism*; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D019831:Sodium-Calcium Exchanger / Q000235:genetics*; D019284:Thapsigargin / Q000494:pharmacology
D007211:Indoles; D007328:Insulin; D019831:Sodium-Calcium Exchanger; C110374:sodium-calcium exchanger 1; D019284:Thapsigargin; C506444:CASP12 protein, human; D053454:Caspase 12; D020169:Caspases; D000252:Calcium-Transporting ATPases; D002118:Calcium; C000543:cyclopiazonic acid