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APO-1(CD95)介导的Jurkat细胞凋亡不涉及src激酶或CD45。

APO-1(CD95)-mediated apoptosis in Jurkat cells does not involve src kinases or CD45.

作者信息

Schraven B, Peter M E

机构信息

Division of Applied Immunology, German Cancer Research Center, Heidelberg.

出版信息

FEBS Lett. 1995 Jul 24;368(3):491-4. doi: 10.1016/0014-5793(95)00720-t.

DOI:10.1016/0014-5793(95)00720-t
PMID:7543423
Abstract

Tyrosine phosphorylation has been reported to be an early event required for APO-1/Fas(CD95) signalling in lymphocytes [Eischen, C.M., Dick, C.J. and Leibson, P.J. (1994) J. Immunol. 153, 1947-1954]. We have compared two mutant Jurkat cells, one largely deficient in expression of CD-45 (J45.01) and a second one deficient in expression of p56lck (JCaM1.6) with wild type Jurkat cells for their ability to undergo APO-1-induced apoptosis. No significant difference was observed among the three cell lines. In the mutant Jurkat cells APO-1 triggering did not result in increased tyrosine phosphorylation of cytosolic proteins. Furthermore, herbimycin A did not inhibit but rather augmented apoptosis at concentrations which effectively degraded the src related kinases lck and fyn. The data suggest that APO-1-mediated signalling is independent from src kinases and CD45.

摘要

据报道,酪氨酸磷酸化是淋巴细胞中APO-1/Fas(CD95)信号传导所需的早期事件[艾申,C.M.,迪克,C.J.和莱布森,P.J.(1994年)《免疫学杂志》153,1947 - 1954]。我们将两种突变的Jurkat细胞与野生型Jurkat细胞进行了比较,一种在很大程度上缺乏CD-45的表达(J45.01),另一种缺乏p56lck的表达(JCaM1.6),比较它们经历APO-1诱导的凋亡的能力。在这三种细胞系之间未观察到显著差异。在突变的Jurkat细胞中,APO-1触发并未导致胞质蛋白酪氨酸磷酸化增加。此外,除莠霉素A在有效降解src相关激酶lck和fyn的浓度下,并未抑制反而增强了凋亡。数据表明,APO-1介导的信号传导独立于src激酶和CD45。

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1
APO-1(CD95)-mediated apoptosis in Jurkat cells does not involve src kinases or CD45.APO-1(CD95)介导的Jurkat细胞凋亡不涉及src激酶或CD45。
FEBS Lett. 1995 Jul 24;368(3):491-4. doi: 10.1016/0014-5793(95)00720-t.
2
Tyrosine phosphorylation-dependent suppression of a voltage-gated K+ channel in T lymphocytes upon Fas stimulation.
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The protein tyrosine kinase inhibitor herbimycin A, but not genistein, specifically inhibits signal transduction by the T cell antigen receptor.蛋白酪氨酸激酶抑制剂赫比霉素A而非染料木黄酮,可特异性抑制T细胞抗原受体的信号转导。
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MHC class I ligation of human T cells activates the ZAP70 and p56lck tyrosine kinases, leads to an alternative phenotype of the TCR/CD3 zeta-chain, and induces apoptosis.人类T细胞的MHC I类分子连接激活ZAP70和p56lck酪氨酸激酶,导致TCR/CD3 ζ链出现另一种表型,并诱导细胞凋亡。
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Immobilized antibodies to CD45 induce rapid morphologic changes and increased tyrosine phosphorylation of p56lck-associated proteins in T cells.固定化的抗CD45抗体可诱导T细胞发生快速形态学变化,并增加与p56lck相关蛋白的酪氨酸磷酸化。
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Tyrosine kinase-dependent activation of a chloride channel in CD95-induced apoptosis in T lymphocytes.酪氨酸激酶依赖性氯离子通道激活在T淋巴细胞CD95诱导的细胞凋亡中的作用
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Use and selectivity of herbimycin A as inhibitor of protein-tyrosine kinases.除草霉素A作为蛋白酪氨酸激酶抑制剂的用途及选择性。
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T cell receptor-induced Fas ligand expression in cytotoxic T lymphocyte clones is blocked by protein tyrosine kinase inhibitors and cyclosporin A.细胞毒性T淋巴细胞克隆中T细胞受体诱导的Fas配体表达被蛋白酪氨酸激酶抑制剂和环孢素A阻断。
Eur J Immunol. 1994 Oct;24(10):2469-76. doi: 10.1002/eji.1830241032.

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Proteinase-activated receptor 1 activation induces epithelial apoptosis and increases intestinal permeability.蛋白酶激活受体1的激活诱导上皮细胞凋亡并增加肠道通透性。
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Fas (CD95) expression and death-mediating function are induced by CD4 cross-linking on CD4+ T cells.
Fas(CD95)的表达及死亡介导功能可通过CD4⁺T细胞上的CD4交联来诱导。
Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11014-8. doi: 10.1073/pnas.93.20.11014.
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EMBO J. 1995 Nov 15;14(22):5579-88. doi: 10.1002/j.1460-2075.1995.tb00245.x.