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槲寄生凝集素I对L1210白血病细胞的内化动力学与细胞毒性之间的关系。

Relationship between internalization kinetics and cytotoxicity of mistletoe lectin I to L1210 leukaemia cells.

作者信息

Walzel H, Jonas L, Rosin T, Brock J

机构信息

Department of Biochemistry, Wilhelm Pieck University, Rostock.

出版信息

Folia Biol (Praha). 1990;36(3-4):181-8.

PMID:2257937
Abstract

We have taken two different approaches to the study of the entry of mistletoe lectin I (MLI) into murine L1210 leukaemia cells. As detected by cellular protein synthesis and DNA synthesis inhibition, the lectin was cytotoxic to L1210 leukaemia cells. Inhibition of [3H]leucine and [3H]thymidine incorporation into L1210 cells by MLI was found dose dependent in a concentration range from 10(-16) to 10(-12) mol/ml. The kinetics of cellular protein synthesis inhibition by MLI was concentration dependent, too. Using preembedding electron microscopy, the binding and intracellular routing of the gold-labelled lectin (MLI.Au15) were studied. MLI was internalized into L1210 leukaemia cells by two different pathways: via coated pits to coated vesicles and via long enclosed invaginations of the plasma membrane.

摘要

我们采用了两种不同的方法来研究槲寄生凝集素I(MLI)进入小鼠L1210白血病细胞的过程。通过细胞蛋白质合成和DNA合成抑制检测发现,该凝集素对L1210白血病细胞具有细胞毒性。在10^(-16)至10^(-12) mol/ml的浓度范围内,发现MLI对L1210细胞中[3H]亮氨酸和[3H]胸苷掺入的抑制呈剂量依赖性。MLI对细胞蛋白质合成的抑制动力学也呈浓度依赖性。利用包埋前电子显微镜,研究了金标记凝集素(MLI.Au15)的结合和细胞内途径。MLI通过两种不同途径内化到L1210白血病细胞中:通过有被小窝进入有被小泡,以及通过质膜的长封闭内陷。

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