Narasimhan V, Holowka D, Baird B
Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.
Biochem Biophys Res Commun. 1990 Aug 31;171(1):222-9. doi: 10.1016/0006-291x(90)91380-b.
Disruption of microfilaments in rat basophilic leukemia (RBL) cells by exposure to cytochalasin B is observed to potentiate the rate of antigen-stimulated secretion from these cells. Under these conditions, cytochalasin B is without effect on the antigen-stimulated production of inositol phosphates or 45Ca2(+)-influx. In streptolysin-O-permeabilized RBL cells, cytochalasin B is observed to potentiate the rate of secretion in response both to guanosine 5'-(2-thio)-O-triphosphate (GTP gamma S) and to Ca2+ (buffered between 0.1 and 10 microM). However, under these conditions, cytochalasin B does not affect to antigen-stimulated production of inositol phosphates. Consistent with these data, microfilaments are proposed to regulate a terminal step in exocytosis, in a physiologically relevant manner.
观察发现,用细胞松弛素B处理大鼠嗜碱性粒细胞白血病(RBL)细胞会破坏微丝,从而增强这些细胞抗原刺激的分泌速率。在这些条件下,细胞松弛素B对抗原刺激的肌醇磷酸生成或45Ca2(+)内流没有影响。在用链球菌溶血素O通透的RBL细胞中,观察到细胞松弛素B能增强对鸟苷5'-(2-硫代)-O-三磷酸(GTPγS)和Ca2+(缓冲在0.1至10微摩尔之间)的分泌速率。然而,在这些条件下,细胞松弛素B不影响抗原刺激的肌醇磷酸生成。与这些数据一致,有人提出微丝以生理相关的方式调节胞吐作用的终末步骤。