摘要
Thapsigargin是内质网Ca^2＋-ATP酶选择性抑制剂，可以不可逆地使内质网钙池排空，使胞质内Ca^2＋浓度持续升高。Thapsigargin诱导细胞发生内质网应激反应并最终发生凋亡。凋亡涉及caspase、细胞核因子κB受体活化因子配体（RANKL）作用的核因子-κB、c—Jun氨基末端激酶等一系列因子。不断深化对thapsigargin的认识，可以为许多疾病的冶疗开辟广阔的前景。
Thapsigargin is a highly selective inhibitor of the endoplasmic reticular Ca^2＋ -dependent ATPase. Thapsigargin is known to deplete intracellular Ca^2＋ stores and induce a sustained Ca^2＋ influx to promote apoptosis in a range of cell types. Apoptosis is associated with caspase-3, RANKL-induced activation of NF-κB, JNK and so on. It＇s wider therapeutic use will be proposed through advanced recognition on thapsigargin.
出处
《国际内分泌代谢杂志》
2007年第2期95-97,共3页
International Journal of Endocrinology and Metabolism
