Fujinaga Yukako
International Research Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Yamada-oka 3-1, Suita, Osaka 565-0871.
J Biochem. 2006 Aug;140(2):155-60. doi: 10.1093/jb/mvj161.
A number of bacterial toxins have sophisticated mechanisms for reaching their specific targets in mammalian cells, to exert their toxicity. This review focuses on the transport mechanisms of cholera toxin and botulinum neurotoxin complex. Cholera toxin is an ADP-ribosyltransferase toxin, and the covalent modification of heterotrimeric Gs protein in the cytosol leads to the activation of adenylyl cyclase and a sequence of events culminating in massive diarrheal disease. Here, we describe the structural features of this toxin and the transport pathway followed by this toxin from the plasma membrane to the cytosol of intestinal epithelial cells. Botulinum neurotoxin is a metalloprotease toxin that enters neurons, where it cleaves core proteins of the neuroexocytosis apparatus and elicits the inhibition of neurotransmitter release. The food-borne botulism is manifested when the neurotoxin is absorbed from the digestive tract, enters the blood stream, and reaches the cytosol of the peripheral nerves. We overview the structural organization and the long journey followed by this toxin.
许多细菌毒素具有复杂的机制，能够抵达哺乳动物细胞中的特定靶点，以发挥其毒性。本综述聚焦于霍乱毒素和肉毒杆菌神经毒素复合物的转运机制。霍乱毒素是一种ADP核糖基转移酶毒素，其对胞质溶胶中异源三聚体Gs蛋白的共价修饰会导致腺苷酸环化酶激活，引发一系列事件，最终导致严重的腹泻病。在此，我们描述了这种毒素的结构特征以及该毒素从质膜到肠上皮细胞胞质溶胶所遵循的转运途径。肉毒杆菌神经毒素是一种金属蛋白酶毒素，它进入神经元后，会切割神经外排装置的核心蛋白，并抑制神经递质释放。当神经毒素从消化道吸收，进入血流并到达外周神经的胞质溶胶时，就会引发食源性肉毒中毒。我们概述了这种毒素的结构组成及其漫长的转运过程。
