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百日咳毒素处理对人自然杀伤细胞功能的影响。

Effects of pertussis toxin treatment on human natural killer cell function.

作者信息

Whalen M M, Doshi R N, Bankhurst A D

机构信息

Department of Medicine, University of New Mexico School of Medicine, Albuquerque 87131.

出版信息

Immunology. 1992 Jul;76(3):402-7.

PMID:1326477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1421690/
Abstract

Membranes from highly purified natural killer (NK) cells were ADP ribosylated by treatment with pertussis toxin (PTX). PTX treatment resulted in a single band of 32P incorporation at M(r) 41,600. PTX treatment of NK cells diminished their ability to lyse K562 tumour cells by about 50%. However PTX treatment had no measurable effect on cAMP levels in NK cells. PTX pretreatment also had no effect on the ability of target cells to induce phosphoinositide turnover or on the ability of the NK cells to conjugate with the K562 tumour cells. Movement toward the chemoattractants interleukin-2 (IL-2) and formylmethionylleucylphenylalanine (FMLP) was significantly inhibited indicating that a PTX substrate in NK cells may be involved in the transduction of signals which are involved in cell motility.

摘要

用百日咳毒素(PTX)处理来自高度纯化的自然杀伤(NK)细胞的膜,可使其发生ADP核糖基化。PTX处理导致在分子量为41,600处出现一条32P掺入带。PTX处理NK细胞使其裂解K562肿瘤细胞的能力降低约50%。然而,PTX处理对NK细胞中的cAMP水平没有可测量的影响。PTX预处理对靶细胞诱导磷酸肌醇周转的能力或NK细胞与K562肿瘤细胞结合的能力也没有影响。向趋化因子白细胞介素-2(IL-2)和甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)的移动受到显著抑制,这表明NK细胞中的一种PTX底物可能参与了与细胞运动相关的信号转导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3982/1421690/eb535dd39c4e/immunology00106-0058-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3982/1421690/eb535dd39c4e/immunology00106-0058-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3982/1421690/eb535dd39c4e/immunology00106-0058-a.jpg

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百日咳毒素胰岛激活蛋白的亚基结构,符合A-B模型。
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Migration of human helper/inducer T cells in response to supernatants from Con A-stimulated suppressor/cytotoxic T cells.人辅助/诱导性T细胞对刀豆蛋白A刺激的抑制/细胞毒性T细胞上清液的迁移反应。
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Coupling of the guanine nucleotide regulatory protein to chemotactic peptide receptors in neutrophil membranes and its uncoupling by islet-activating protein, pertussis toxin. A possible role of the toxin substrate in Ca2+-mobilizing receptor-mediated signal transduction.中性粒细胞膜中鸟嘌呤核苷酸调节蛋白与趋化肽受体的偶联及其被胰岛激活蛋白(百日咳毒素)解偶联。毒素底物在钙离子动员受体介导的信号转导中的可能作用。
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