| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
Cell lines | HEK293 cells |
Preparation Method | No-tagged MS4A12 and GCaMP-MS4A12 plasmids were mixed at a 1:1 ratio and then transfected into HEK293 cells grown on coverslips.Thapsigargin of 5 μM was used for stimulation and store depletion, after which 5 mM Ca2+regular solution was perfused to visualize Ca2+influx-induced fluorescence of GCaMP-MS4A12. |
Reaction Conditions | 5 μM; 37℃ |
Applications | When cells were stimulated with a store-depleting condition (5 μM thapsigargin for 5 min in the 5 mM Ca2+extracellular solution), the fluorescence of GCaMP-M12 very rapidly and greatly increased. |
Animal models | 6- to 8-week-old BALB/c mice (female) |
Preparation Method | The mice were intranasally infected with 3 MLD50 of PR8/H1N1 virus. Twelve hours post-infection, Thapsigargin (1.5 μg/kg/day), oseltamivir (45 mg/kg/day) or PBS+DMSO (percentage DMSO in PBS-DMSO control equal to other treatments) was orally administered by gavage daily for 5 days. At 3 and 5 days post-infection, the lungs of four mice from each group were collected for viral titration. |
Dosage form | 1.5 μg/kg/day; p.o. |
Applications | The Thapsigargin-treated group showed significantly improved survival, reduced virus shedding at 3 and 5 days post-infection and less severe weight loss. |
| 文献引用 | |
| 产品描述 | Thapsigargin is an inhibitor of the sarcoplasmic/endoplasmic reticulum Ca2+ATPase pump.[1]Thapsigargin can induce a potent host antiviral response that blocks influenza A virus replication at nano-molar non-cytotoxic levels.[2] In vitro efficacy test it shown that HEp2 cells primed with 0.5 μM Thapsigargin (as a non-cytotoxic inhibitor) before infection reduced progeny virus production by almost 10,000-fold. A549 cells primed with 0.3 μM Thapsigargin, in turn, was more inhibitory than the RDV-treated cells by 450-fold.[3]In vitro, treatment with 10 μM of Thapsigargin (a specific blocker SERCAs), can null EMF response by impairing the replenishment of the ER.[4]In vitro test it indicated that treatment with 0.001 μM - 1 μM of thapsigargin may arrest cell proliferations in MH7A human rheumatoid arthritis synovial cells in a time- and dose-dependent manner.[5]Treatment with 1 μM of thapsigargin mediated sensitization to TRAIL in ESCC cell lines through the activation of AMPK from the aspects of protein function and existence.[7] In vivo efficacy study it demonstrated that treatment with 0.5ug/g/body weight of Thapsigargin was safe and did not elicit any adverse effects on survival in mice.[6]In vivo, mice were treated with 1 mg/kg thapsigargin and 60 mg/kg hrTRAIL intraperitoneally for five times per week, improved the expression of CHOP, increased AMPK phosphorylation, increased the expression of DR5, increased the expression of Bax, and activated Caspase 9, while suppressing Bcl2 expression.[7] References: |
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