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神经节苷脂功能性整合入完整细胞:霍乱毒素反应性的诱导

Functional incorporation of ganglioside into intact cells: induction of choleragen responsiveness.

作者信息

Moss J, Fishman P H, Manganiello V C, Vaughan M, Brady R O

出版信息

Proc Natl Acad Sci U S A. 1976 Apr;73(4):1034-7. doi: 10.1073/pnas.73.4.1034.

Abstract

NCTC 2071 cells are unable to synthesize the monosialoganglioside GM1. When grown in chemically defined medium these cells contained no detectable GM1 and did not accumulate 3': 5'-cyclic AMP in response to choleragen. Incubation of the cells with [3H]GM1 permitted quantification of ganglioside uptake which was dependent on time and concentration of [3H]GM1 in the medium. Responsiveness to choleragen was demonstrated with binding of as few as 17,000 molecules of [3H]GM1 per cell; a maximal response was observed with 10(5) molecules per cell. With increasing cellular content of GM1, the rate of rise in intracellular cyclic AMP in response to choleragen was increased. With greater than 1 X 10(5) molecules of GM1 per cell, the delay between addition of choleragen and the cyclic AMP response was inversely proportional to choleragen concentration; less than 250 molecules of choleragen per cell caused a significant increase in cyclic AMP after 8 hr of incubation. Although the responsiveness of intact cells to choleragen was dependent on GM1, choleragen activation of adenylate cyclase in homogenates with 0.6 mM NAD was independent of added ganglioside. These observations are consistent with the view that exogenous ganglioside GM1 can be functionally integrated into the surface membrane of intact cells and serve as the choleragen receptor. Furthermore, although exogenous GM1 is required for choleragen responsiveness in intact cells, the ganglioside does not play an obligatory role in cell homogenates, where the surface receptor can presumably be bypassed.

摘要

NCTC 2071细胞无法合成单唾液酸神经节苷脂GM1。当在化学成分明确的培养基中培养时,这些细胞不含可检测到的GM1,并且对霍乱毒素不积累3':5'-环磷酸腺苷。用[3H]GM1孵育细胞可对神经节苷脂摄取进行定量,其摄取量取决于培养基中[3H]GM1的时间和浓度。每个细胞仅结合17,000个[3H]GM1分子就能证明对霍乱毒素有反应;每个细胞结合10(5)个分子时观察到最大反应。随着细胞内GM1含量的增加,对霍乱毒素反应时细胞内环磷酸腺苷的上升速率增加。当每个细胞的GM1分子数大于1×10(5)时,添加霍乱毒素与环磷酸腺苷反应之间的延迟与霍乱毒素浓度成反比;每个细胞少于250个霍乱毒素分子在孵育8小时后会导致环磷酸腺苷显著增加。尽管完整细胞对霍乱毒素的反应性依赖于GM1,但在含有0.6 mM NAD的匀浆中,霍乱毒素对腺苷酸环化酶的激活与添加的神经节苷脂无关。这些观察结果与以下观点一致,即外源性神经节苷脂GM1可以在功能上整合到完整细胞的表面膜中并作为霍乱毒素受体。此外,尽管完整细胞对霍乱毒素的反应性需要外源性GM1,但神经节苷脂在细胞匀浆中并不起必需作用,在细胞匀浆中表面受体大概可以被绕过。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2937/430194/e0963d9629bd/pnas00034-0061-a.jpg

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