Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.     

挠率几何与有挠引力

本文提出一种统一描述引力场、规范场及自旋自相互作用的纤维丛理论.它把现有的挠率概念包含在其中,如Cartan理论、Brans-Dicke理论、规范引力理论等.本文还给出了一种拉伸纤维的映射,它为进一步探讨挠率产生的几何机制和物理机制提供了新的研究方式.     

N-烷基-O-烷基-O-(1,2,2,2-四氯乙基)硫代磷酰胺酯的合成研究

合成了9个未见文献报导的四氯乙基硫代磷酰胺酯,并对它们的合成、结构和性质以及杀蚜虫、线虫活性等进行了初步研究。     

非马尔科夫多值噪声驱动下系统的平均第一通过时间

本文把Weiss等发展的计算平均第一通过时间(简称MFPT)的新方法推广到由非马尔科夫多值噪声驱动的过程.为了简化,本文只限于研究矩形分布这一情形.通过一个重要实例,对MFPT进行了具体计算,并得到了显式解析表示.     

丙酮缩二甲醇的合成及应用

介绍了丙酮缩二甲醇的合成方法及其主要用途,概要地报道了合成丙酮缩乙二醇及以此为原料合成丙酮缩二甲醇的新工艺。     

产品原理方案的功能设计法──“管接头标记自动压印机”的原理方案设计

本文通过“管接头标记自动压印机”原理方案的构思过程，说明产品原理方案设计的功能论方法的一般原理和特点及其应用。     

Retrograde transport of endocytosed Shiga toxin to the endoplasmic reticulum.

Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol.