BIOSYNTHESIS AND FUNCTION OF GLYCOSPHINGOLIPIDS AND OTHER GLYCOCONJUGATES

神经节苷脂似乎是细胞上的重要识别分子 表面，并被认为是某些细菌毒素的受体 和病毒。 然而，人们对正常的生理 这些质膜成分的作用。 我们已经开发出多种 方法和模型系统来解决这个问题。 荧光衍生物 含有罗丹明或荧光黄CH的神经节苷脂GM 1的含量为 合成并显示与天然GM 1一样有效， 霍乱毒素 将荧光神经节苷脂插入血浆中， 小鼠和大鼠胸腺细胞的膜，并在细胞 暴露于霍乱毒素或抗罗丹明抗体，这两者都是 多价的。 霍乱毒素还可诱导内源性细胞膜的修补和封盖。 胸腺细胞表面的GM 1。 大鼠胸腺细胞暴露于B或 毒素的结合亚基导致增殖反应， 通过增加DNA合成来衡量。 即使在25 ng/M1时，B亚基也是 有效作为促分裂剂。 B亚单位与抗霍乱药预先孵育 毒素抗体阻断了它与细胞的结合和对细胞的刺激。 B亚基作为有丝分裂原是有效的。 B的预先孵育 抗霍乱毒素抗体的亚基阻断了它与 刺激细胞。 显示B亚基不含任何 腺苷酸环化酶激活A亚单位;环AMP抑制 有丝分裂 因此，几种GM 1分子在胸腺细胞上的结合 通过B亚单位的表面导致跨血浆的转导 有丝分裂信号的膜。

Gangliosides appear to be important recognition molecules on the cell surface and have been implicated as receptors for certain bacterial toxins and viruses. Little is known, however, about the normal physiological role(s) of these plasma membrane components. We have developed several approaches and model sysems to address this issue. Fluorescent derivatives of ganglioside GM1 containing either rhodamine or Lucifer yellow CH were synthesized and shown to be as effective as native GM1 as receptors for cholera toxin. The fluorescent gangliosides were inserted into the plasma membrane of mouse and rat thymocytes and underwent capping when the cells were exposed to cholera toxin or anti-rhodamine antibodies, which are both multivalent. Cholera toxin also induced patching and capping of endogenous GM1 on the thymocyte surface. Exposure of rat thymocytes to the B or binding subunit of the toxin resulted in a proliferative response as measured by increased DNA synthesis. Even at 25 ng/M1, the B subunit was effective as a mitogen. Prior incubation of the B subunit with anticholera toxin antibodies blocked both its binding to and stimulation of the cells. The B subunit was effective as a mitogen. Prior incubation of the B subunit with anticholera toxin antibodies blocked both its binding to and stimulation of the cells. The B subunit was shown to be free of any adenylate cyclase-activating A subunit; and cyclic AMP inhibited mitogenesis. Thus, binding of several molecules of GM1 on the thymocyte surface by the B subunit leads to the transduction across the plasma membrane of a mitogenic signal.