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Overview
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Background
Thapsigargin is an inhibitor of microsomal Ca2+-ATPase, Thapsigargin inhibits the carbachol-evoked [Ca2+]i-transients with IC50 value of 0.353 nM[1].
Thapsigargin may induce cell apoptosis in MH7A cells in a time- and dose-dependent manner, and the percentages of cell death reached 44.6% at thapsigargin concentration of 1 μM treated for 4 days compared to the control. The protein and mRNA levels of cyclin D1 decreased gradually with the increasing of thapsigargin concentration and treatment times[2].
In regards to vivo results, tunicamycin is superior in not only inducing ER stress but also recapturing the metabolic alterations associated with ER stress[3].[1]. Garavito-Aguilar ZV, et al. Differential thapsigargin-sensitivities and interaction of Ca2+ stores in human SH-SY5Y neuroblastoma cells. Brain Res. 2004 Jun 18;1011(2):177-86.
[2]. Wang H, et al. Effects of thapsigargin on the proliferation and survival of human rheumatoid arthritis synovialcells. ScientificWorldJournal. 2014 Feb 9;2014:605416.
[3]. Abdullahi A, et al. Modeling Acute ER Stress in Vivo and in Vitro. Shock. 2017 Apr;47(4):506-513.
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