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一种改变碳水化合物结合蛋白功能的突变会阻碍盘基网柄菌发育过程中的细胞间黏附。

A mutation altering the function of a carbohydrate binding protein blocks cell-cell cohesion in developing Dictyostelium discoideum.

作者信息

Ray J, Shinnick T, Lerner R

出版信息

Nature. 1979 May 17;279(5710):215-21. doi: 10.1038/279215a0.

Abstract

In Dictyostelium discoideum, carbohydrate binding proteins (CBPs) or lectins have been implicated in the molecular basis of cellular cohesion. To determine the role of these CBPs, we have attempted to isolate structural gene mutants in which the CBPs have a defective affinity for carbohydrate ligands. We now report the isolation of a spontaneous, cross-reacting material (CRM) mutant which is non-cohesive and fails to develop. The mutant seems to have a defect in the structural gene for one of the two developmentally regulated carbohydrate binding proteins (CBP-26), which renders it unable to bind to galactose-containing ligands. The fact that wild-type cells interact with the mutant and carry it through development strongly supports a model of cell-cell interaction in which cohesion is mediated by complementary molecules.

摘要

在盘基网柄菌中,碳水化合物结合蛋白(CBPs)或凝集素与细胞黏附的分子基础有关。为了确定这些CBPs的作用,我们试图分离出结构基因突变体,其中CBPs对碳水化合物配体的亲和力存在缺陷。我们现在报告分离出一种自发的交叉反应物质(CRM)突变体,它没有黏附性且无法发育。该突变体似乎在两种发育调控的碳水化合物结合蛋白(CBP - 26)之一的结构基因中存在缺陷,这使其无法与含半乳糖的配体结合。野生型细胞与突变体相互作用并携带其完成发育,这一事实有力地支持了一种细胞间相互作用模型,即黏附是由互补分子介导的。

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