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将神经节苷脂GM1导入大鼠胶质瘤C6细胞,会使其对霍乱毒素B亚基的生长抑制作用敏感。

Insertion of ganglioside GM1 into rat glioma C6 cells renders them susceptible to growth inhibition by the B subunit of cholera toxin.

作者信息

Spiegel S

机构信息

Membrane Biochemistry Section, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD.

出版信息

Biochim Biophys Acta. 1988 May 13;969(3):249-56. doi: 10.1016/0167-4889(88)90059-6.

Abstract

The B subunit of cholera toxin does not affect the growth of rat glioma C6 cells which are deficient of its receptor, ganglioside GM1. Insertion of ganglioside GM1 into the plasma membrane of C6 cells renders them susceptible to inhibition of DNA synthesis by the B subunit. Exposure of C6 cells to butyrate induces an elevation of ganglioside GM1 as measured by an increase in binding of iodinated cholera toxin and also results in an inhibition of DNA synthesis by the B subunit. The extent of inhibition of DNA synthesis correlated with the binding of B subunit and was independent of adenylate cyclase activation or increases in intracellular cAMP levels.

摘要

霍乱毒素的B亚基不会影响缺乏其受体神经节苷脂GM1的大鼠胶质瘤C6细胞的生长。将神经节苷脂GM1插入C6细胞的质膜会使其易受B亚基对DNA合成的抑制作用影响。用丁酸处理C6细胞会导致神经节苷脂GM1升高,这可通过碘化霍乱毒素结合增加来衡量,同时也会导致B亚基抑制DNA合成。DNA合成的抑制程度与B亚基的结合相关,且与腺苷酸环化酶激活或细胞内cAMP水平升高无关。

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