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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Gusovsky F, Yasumoto T, Daly J W

Laboratory of Bioorganic Chemistry, NIDDK, Bethesda, Maryland 20892.

Cell Mol Neurobiol. 1987 Sep;7(3):317-22. doi: 10.1007/BF00711308.

Maitotoxin (MTX) was an extraordinarily potent stimulant of phosphoinositide breakdown in the neuroblastoma hybrid NCB-20 cells. 2. Maximal responses were obtained at 0.25-0.5 ng MTX/ml, and resulted in increased formation of [3H]inositol mono-, bis-, and trisphosphates. Increased formation of [3H]inositol bis- and trisphosphate was observed as early as 15 sec after the addition of MTX. 3. MTX-induced phosphoinositide breakdown in NCB-20 cells was not antagonized by organic (nifedipine, methoxyverapamil) or inorganic (Mn2+, Co2+, Cd2+) calcium channel blockers. However, the response on phosphoinositide breakdown was completely eliminated in the absence of extracellular calcium. 4. The results suggest that MTX either directly stimulates phosphoinositide breakdown in a calcium-dependent manner or acts indirectly through calcium channels insensitive to organic/inorganic calcium channel blockers.

maitotoxin（MTX）是神经母细胞瘤杂交细胞NCB - 20中磷酸肌醇分解的一种极其有效的刺激物。2. 在0.25 - 0.5 ng MTX/ml时获得最大反应，导致[3H]肌醇单磷酸、双磷酸和三磷酸的生成增加。早在加入MTX后15秒就观察到[3H]肌醇双磷酸和三磷酸的生成增加。3. NCB - 20细胞中MTX诱导的磷酸肌醇分解不受有机（硝苯地平、甲氧维拉帕米）或无机（Mn2 +、Co2 +、Cd2 +）钙通道阻滞剂的拮抗。然而，在没有细胞外钙的情况下，对磷酸肌醇分解的反应完全消除。4. 结果表明，MTX要么以钙依赖的方式直接刺激磷酸肌醇分解，要么通过对有机/无机钙通道阻滞剂不敏感的钙通道间接起作用。

Gusovsky F, Yasumoto T, Daly J W

Laboratory of Bioorganic Chemistry, NIDDK, Bethesda, Maryland 20892.

Cell Mol Neurobiol. 1987 Sep;7(3):317-22. doi: 10.1007/BF00711308.

Maitotoxin (MTX) was an extraordinarily potent stimulant of phosphoinositide breakdown in the neuroblastoma hybrid NCB-20 cells. 2. Maximal responses were obtained at 0.25-0.5 ng MTX/ml, and resulted in increased formation of [3H]inositol mono-, bis-, and trisphosphates. Increased formation of [3H]inositol bis- and trisphosphate was observed as early as 15 sec after the addition of MTX. 3. MTX-induced phosphoinositide breakdown in NCB-20 cells was not antagonized by organic (nifedipine, methoxyverapamil) or inorganic (Mn2+, Co2+, Cd2+) calcium channel blockers. However, the response on phosphoinositide breakdown was completely eliminated in the absence of extracellular calcium. 4. The results suggest that MTX either directly stimulates phosphoinositide breakdown in a calcium-dependent manner or acts indirectly through calcium channels insensitive to organic/inorganic calcium channel blockers.

maitotoxin（MTX）是神经母细胞瘤杂交细胞NCB - 20中磷酸肌醇分解的一种极其有效的刺激物。2. 在0.25 - 0.5 ng MTX/ml时获得最大反应，导致[3H]肌醇单磷酸、双磷酸和三磷酸的生成增加。早在加入MTX后15秒就观察到[3H]肌醇双磷酸和三磷酸的生成增加。3. NCB - 20细胞中MTX诱导的磷酸肌醇分解不受有机（硝苯地平、甲氧维拉帕米）或无机（Mn2 +、Co2 +、Cd2 +）钙通道阻滞剂的拮抗。然而，在没有细胞外钙的情况下，对磷酸肌醇分解的反应完全消除。4. 结果表明，MTX要么以钙依赖的方式直接刺激磷酸肌醇分解，要么通过对有机/无机钙通道阻滞剂不敏感的钙通道间接起作用。