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1
Fusicoccin Counteracts the n-Ethylmaleimide and Silver-Induced Stimulation of Oxygen Uptake in Egeria densa Leaves.藤霉素可抵消N-乙基马来酰亚胺和银诱导的伊乐藻叶片氧气吸收刺激作用。
Plant Physiol. 1998 Feb 1;116(2):681-6. doi: 10.1104/pp.116.2.681.
2
The respiratory burst and electrolyte leakage induced by sulfhydryl blockers in egeria densa leaves are associated with H2O2 production and are dependent on Ca2+ influx.巯基阻断剂诱导的伊乐藻叶片呼吸爆发和电解质渗漏与过氧化氢的产生有关,并依赖于钙离子内流。
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3
Inhibition of catalase activity as an early response of Arabidopsis thaliana cultured cells to the phytotoxin fusicoccin.过氧化氢酶活性的抑制作为拟南芥培养细胞对植物毒素壳梭孢菌素的早期反应。
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Effect of cutting on solute uptake by plasma membrane vesicles from sugar beet (Beta vulgaris L.) leaves.切割对甜菜(Beta vulgaris L.)叶片质膜囊泡溶质摄取的影响。
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Fusicoccin-induced catalase inhibitor is produced independently of H+-ATPase activation and behaves as an organic acid.福司可林诱导的过氧化氢酶抑制剂的产生与 H+-ATPase 的激活无关,并且表现为有机酸。
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Fusicoccin Binding to Its Plasma Membrane Receptor and the Activation of the Plasma Membrane H+-ATPase (III. Is There a Direct Interaction between the Fusicoccin Receptor and the Plasma Membrane H+-ATPase?).壳梭孢菌素与其质膜受体的结合及质膜H⁺-ATP酶的激活(III. 壳梭孢菌素受体与质膜H⁺-ATP酶之间是否存在直接相互作用?)
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Soluble and insoluble immune complexes activate human neutrophil NADPH oxidase by distinct Fc gamma receptor-specific mechanisms.可溶性和不溶性免疫复合物通过不同的Fcγ受体特异性机制激活人中性粒细胞NADPH氧化酶。
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Characterization of essential sulfhydryl groups of rat renal Na(+)-Pi cotransporter.大鼠肾脏钠-磷酸盐共转运体必需巯基基团的特性研究
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引用本文的文献

1
The respiratory burst and electrolyte leakage induced by sulfhydryl blockers in egeria densa leaves are associated with H2O2 production and are dependent on Ca2+ influx.巯基阻断剂诱导的伊乐藻叶片呼吸爆发和电解质渗漏与过氧化氢的产生有关,并依赖于钙离子内流。
Plant Physiol. 1998 Dec;118(4):1379-87. doi: 10.1104/pp.118.4.1379.

本文引用的文献

1
Phloem loading in Vicia faba leaves: Effect of N-ethylmaleimide and parachloromercuribenzenesulfonic acid on H(+) extrusion, K (+) and sucrose uptake.蚕豆叶片韧皮部装载:N-乙基马来酰亚胺和对氯汞苯甲酸对 H(+)外排、K (+)和蔗糖摄取的影响。
Planta. 1980 Jul;149(2):144-8. doi: 10.1007/BF00380875.
2
Fungal elicitors induce a transient release of active oxygen species from cultured spruce cells that is dependent on Ca(2+) and protein-kinase activity.真菌诱导物诱导培养云杉细胞瞬时释放活性氧,该过程依赖于 Ca(2+) 和蛋白激酶活性。
Planta. 1992 Apr;187(1):136-41. doi: 10.1007/BF00201635.
3
Involvement of plasma membrane calcium influx in bacterial induction of the k/h and hypersensitive responses in tobacco.质膜钙内流参与细菌诱导烟草中的K/H和过敏反应。
Plant Physiol. 1990 Jan;92(1):215-21. doi: 10.1104/pp.92.1.215.
4
Plasmalemma Redox Chain and H Extrusion: II. Respiratory and Metabolic Changes Associated with Fusicoccin-Induced and with Ferricyanide-Induced H Extrusion.质膜氧化还原链和 H 外排:II. 与 fusicoccin 诱导的和与铁氰化物诱导的 H 外排相关的呼吸和代谢变化。
Plant Physiol. 1988 May;87(1):30-5. doi: 10.1104/pp.87.1.30.
5
Electrogenic sucrose transport in developing soybean cotyledons.在发育中的大豆子叶中电致蔗糖转运。
Plant Physiol. 1981 Apr;67(4):869-74. doi: 10.1104/pp.67.4.869.
6
Plasma Membrane Redox Enzyme Is Involved in the Synthesis of O2- and H2O2 by Phytophthora Elicitor-Stimulated Rose Cells.质膜氧化还原酶参与疫霉激发子刺激的玫瑰细胞中O2-和H2O2的合成。
Plant Physiol. 1995 Apr;107(4):1241-1247. doi: 10.1104/pp.107.4.1241.
7
Fusicoccin Binding to Its Plasma Membrane Receptor and the Activation of the Plasma Membrane H+-ATPase (III. Is There a Direct Interaction between the Fusicoccin Receptor and the Plasma Membrane H+-ATPase?).壳梭孢菌素与其质膜受体的结合及质膜H⁺-ATP酶的激活(III. 壳梭孢菌素受体与质膜H⁺-ATP酶之间是否存在直接相互作用?)
Plant Physiol. 1996 Mar;110(3):957-964. doi: 10.1104/pp.110.3.957.
8
Elicitor-stimulated ion fluxes and O2- from the oxidative burst are essential components in triggering defense gene activation and phytoalexin synthesis in parsley.激发子刺激的离子通量和氧化爆发产生的超氧阴离子是引发欧芹中防御基因激活和植保素合成的重要组成部分。
Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4800-5. doi: 10.1073/pnas.94.9.4800.
9
Phosphorylated nitrate reductase from spinach leaves is inhibited by 14-3-3 proteins and activated by fusicoccin.菠菜叶片中的磷酸化硝酸还原酶受14-3-3蛋白抑制,并被壳梭孢菌素激活。
Curr Biol. 1996 Sep 1;6(9):1104-13. doi: 10.1016/s0960-9822(02)70677-5.
10
Calcium-mediated apoptosis in a plant hypersensitive disease resistance response.钙介导的植物过敏反应性抗病反应中的细胞凋亡
Curr Biol. 1996 Apr 1;6(4):427-37. doi: 10.1016/s0960-9822(02)00510-9.

藤霉素可抵消N-乙基马来酰亚胺和银诱导的伊乐藻叶片氧气吸收刺激作用。

Fusicoccin Counteracts the n-Ethylmaleimide and Silver-Induced Stimulation of Oxygen Uptake in Egeria densa Leaves.

作者信息

Albergoni F

机构信息

Centro di Studio del Consiglio Nazionale delle Richerche sulla Biologia Cellulare e Molecolare delle piante (M.T.M.), Università di Milano (F.A.), via Celoria 26, 20133 Milano, Italy

出版信息

Plant Physiol. 1998 Feb 1;116(2):681-6. doi: 10.1104/pp.116.2.681.

DOI:10.1104/pp.116.2.681
PMID:9490768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC35126/
Abstract

It was previously shown that a number of sulfhydryl [SH] group reagents (N-ethylmaleimide [NEM], iodoacetate, Ag+, HgCl2, etc.) can induce a marked, transitory stimulation of O2 uptake (QO2) in Egeria densa leaves, insensitive to CN- and salicylhydroxamic acid and inhibited by diphenylene iodonium and quinacrine. The phytotoxin fusicoccin (FC) also induces a marked increase in O2 consumption in E. densa leaves, apparently independent of the recognized stimulating action on the H+-ATPase. In this investigation we compared the FC-induced increase in O2 consumption with those induced by NEM and Ag+, and we tested for a possible interaction between FC and the two SH blockers in the activation of QO2. The results show (a) the different nature of the FC- and NEM- or Ag+-induced increases of QO2; (b) that FC counteracts the NEM- (and Ag+)-induced respiratory burst; and (c) that FC strongly reduces the damaging effects on plasma membrane permeability observed in E. densa leaves treated with the two SH reagents. Two alternative models of interpretation of the action of FC, in activating a CN--sensitive respiratory pathway and in suppressing the SH blocker-induced respiratory burst, are proposed.

摘要

先前的研究表明,许多巯基[SH]基团试剂(N - 乙基马来酰亚胺[NEM]、碘乙酸、Ag⁺、HgCl₂等)可诱导伊乐藻叶片中氧气吸收(QO₂)显著且短暂的刺激,这种刺激对氰化物和水杨羟肟酸不敏感,但受二苯撑碘鎓和奎纳克林抑制。植物毒素藤霉素(FC)也可诱导伊乐藻叶片中氧气消耗显著增加,这显然独立于其对H⁺ - ATP酶的公认刺激作用。在本研究中,我们比较了FC诱导的氧气消耗增加与NEM和Ag⁺诱导的增加,并测试了FC与两种SH阻断剂在激活QO₂过程中可能的相互作用。结果表明:(a)FC、NEM或Ag⁺诱导的QO₂增加性质不同;(b)FC可抵消NEM(和Ag⁺)诱导的呼吸爆发;(c)FC可强烈降低用两种SH试剂处理的伊乐藻叶片中观察到的对质膜通透性的损伤作用。提出了两种关于FC作用的替代解释模型,一种是激活对氰化物敏感的呼吸途径,另一种是抑制SH阻断剂诱导的呼吸爆发。