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B淋巴细胞受体与多磷酸肌醇降解

B lymphocyte receptors and polyphosphoinositide degradation.

作者信息

Bijsterbosch M K, Meade C J, Turner G A, Klaus G G

出版信息

Cell. 1985 Jul;41(3):999-1006. doi: 10.1016/s0092-8674(85)80080-5.

Abstract

Resting B lymphocytes can be activated and induced to proliferate by antibodies against their antigen receptors (anti-lg). We demonstrate an early increase in the level of [3H]inositol trisphosphate in [3H]inositol-labeled murine B cells, which suggests breakdown of phosphatidylinositol bisphosphate by phospholipase C. In line with this, the level of [3H]1,2-diacylglycerol was also elevated after incubation of [3H]arachidonic-acid-labeled B cells with anti-Ig. Anti-lg also caused a rapid increase in the level of cytosolic Ca2+ in B cells. In contrast, two other polyclonal B cell activators, lipopolysaccharide and phorbol myristate acetate, failed to induce any of these effects. Our results suggest that anti-lg may induce B cell growth via phosphoinositide degradation and Ca2+ mobilization, and that phorbol myristate acetate, and possibly lipopolysaccharide, bypass these initial events.

摘要

静息B淋巴细胞可被针对其抗原受体的抗体(抗Ig)激活并诱导增殖。我们证明,在[³H]肌醇标记的小鼠B细胞中,[³H]肌醇三磷酸水平早期升高,这表明磷脂酰肌醇二磷酸被磷脂酶C分解。与此一致的是,在用抗Ig孵育[³H]花生四烯酸标记的B细胞后,[³H]1,2 - 二酰基甘油水平也升高。抗Ig还导致B细胞胞质Ca²⁺水平迅速升高。相比之下,另外两种多克隆B细胞激活剂脂多糖和佛波醇肉豆蔻酸酯未能诱导出这些效应中的任何一种。我们的结果表明,抗Ig可能通过磷酸肌醇降解和Ca²⁺动员诱导B细胞生长,而佛波醇肉豆蔻酸酯以及可能的脂多糖绕过了这些初始事件。

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