Pharmacological studies on bioactive compounds isolated from marine organisms

Goniodomin已经显示出由于活性因子到修饰活性因子蛋白酶活性的转化变化。这种化合物增加和减少的活性蛋白ATP酶活性，可能通过刺激和抑制性网站在活性上，尊重。肌钙蛋白/肌钙蛋白复合体绑定以抑制活性的Goniodomin A-诱导的活性蛋白ATP酶活性的增强，可能是由分子上影响刺激位点的。Xestoquinone， isolated from a sea sponge Xestospongia sapra， caused a concentration-dependent Ca y D12+ y D1 release through sulfhydryl modification from skeletal muscle sarcoplasmic rericulum。5，6-Dibromo-1，2-dimethylgramine evoked Ca-D12 + D1 release from skeletal muscle sarcoplasmic reticulum through ryanodine receptors in a concentration-dependent maner。Study of structure-activity relationship for Ca D12+ Ca D1 release indicated that 1-methylation and/or both5-and 6-bromination are important for Ca D12+ Ca D1 release。Maitotoxin induced a profound increase in Ca D12+ Ca D1 influx in an extracellular Ca D12+ Ca D1-dependent manner。Maitotoxin作为A-23187和双丁二烯环AMP利用了C6-BU-1细胞中神经生长因子（NGF）的加速生产，由NGF酶免疫测定。Maitotoxin activated a voltage-insensitive Ca-D12 + Ca-D1 channel and accelerated NGF production mediated through a Ca-D12 + Ca-D1 signaling pathway in C6-BU-1 glioma cells。Amphidinolide B增强了活性素和肌钙蛋白直接和增加的Ca-D12 + Y-D1通过肌钙蛋白/肌钙蛋白系统介导的Contractile Apparatus敏感性，结果在ATP酶活性中的增加和增强肌钙蛋白的契约反应。

Goniodomin A has been shown to cause the conformational change of actin to modify actomyosin ATPase activity. This compound increased and decreased actomyosin ATPase activity, probably through the stimulatory and inhibitory sites on actin, respectively. The troponin/tropomyosin complex binds to actin to inhibit the goniodomin A-induced enhancement of actomyosin ATPase activity, probably by the affecting the stimulatory site on the molecule. Xestoquinone, isolated from a sea sponge Xestospongia sapra, caused a concentration-dependent CaィイD12+ィエD1 release through sulfhydryl modification from skeletal muscle sarcoplasmic rericulum. 5,6-Dibromo-1,2-dimethylgramine evoked CaィイD12+ィエD1 release from skeletal muscle sarcoplasmic reticulum through ryanodine receptors in a concentration-dependent manner. Study of structure-activity relationship for CaィイD12+ィエD1 release indicated that 1-methylation and/or both 5- and 6-bromination are important for CaィイD12+ィエD1 release. Maitotoxin induced a profound increase in CaィイD12+ィエD1 influx in an extracellular CaィイD12+ィエD1-dependent manner. Maitotoxin as well as A-23187 and dubutyryl cyclic AMP caused an acceleration of nerve growth factor (NGF) production in C6-BU-1 cells, as determined by NGF enzyme immunoassay. Maitotoxin activated a voltage-insensitive CaィイD12+ィエD1 channel and accelerated NGF production mediated through a CaィイD12+ィエD1 signaling pathway in C6-BU-1 glioma cells. Amphidinolide B enhanced an interaction of actin and myosin directly and increased CaィイD12+ィエD1 sensitivity of the contractile apparatus mediated through troponin/tropomyosin system, resulting in an increase in the ATPase activity and thus enhanced the contractile response of myofilament.