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本文引用的文献

1
Post-transcriptional regulation of GORK channels by superoxide anion contributes to increases in outward-rectifying K⁺ currents.超氧阴离子对 GORK 通道的转录后调节导致外向整流钾电流增加。
New Phytol. 2013 Jun;198(4):1039-1048. doi: 10.1111/nph.12226. Epub 2013 Mar 20.
2
A role for oxalic acid generation in ozone-induced signallization in Arabidopis cells.草酸生成在拟南芥细胞臭氧诱导信号转导中的作用。
Plant Cell Environ. 2013 Mar;36(3):569-78. doi: 10.1111/j.1365-3040.2012.02596.x. Epub 2012 Sep 7.
3
Regulating the reapers: activating metacaspases for programmed cell death.调控收割者:激活效应子半胱天冬酶引发程序性细胞死亡。
Trends Plant Sci. 2012 Aug;17(8):487-94. doi: 10.1016/j.tplants.2012.05.003. Epub 2012 Jun 2.
4
Metacaspases.半胱天冬酶
Cell Death Differ. 2011 Aug;18(8):1279-88. doi: 10.1038/cdd.2011.66. Epub 2011 May 20.
5
Morphological classification of plant cell deaths.植物细胞死亡的形态分类。
Cell Death Differ. 2011 Aug;18(8):1241-6. doi: 10.1038/cdd.2011.36. Epub 2011 Apr 15.
6
Dihydrosphingosine-induced programmed cell death in tobacco BY-2 cells is independent of H₂O₂ production.二氢神经酰胺诱导烟草 BY-2 细胞程序性死亡不依赖于 H₂O₂的产生。
Mol Plant. 2011 Mar;4(2):310-8. doi: 10.1093/mp/ssq077. Epub 2011 Jan 3.
7
Increased anion channel activity is an unavoidable event in ozone-induced programmed cell death.增加阴离子通道活性是臭氧诱导程序性细胞死亡中不可避免的事件。
PLoS One. 2010 Oct 13;5(10):e13373. doi: 10.1371/journal.pone.0013373.
8
Apoptotic-like programmed cell death in plants.植物中类凋亡程序性细胞死亡
New Phytol. 2008;180(1):13-26. doi: 10.1111/j.1469-8137.2008.02549.x.
9
Cell shrinkage and monovalent cation fluxes: role in apoptosis.细胞皱缩与单价阳离子通量:在细胞凋亡中的作用
Arch Biochem Biophys. 2007 Jun 15;462(2):176-88. doi: 10.1016/j.abb.2007.01.020. Epub 2007 Feb 8.
10
Mitochondrial membrane permeabilization in cell death.细胞死亡中的线粒体膜通透性改变
Physiol Rev. 2007 Jan;87(1):99-163. doi: 10.1152/physrev.00013.2006.

臭氧诱导的半胱天冬酶样活性依赖于拟南芥细胞早期的离子通道调节和 ROS 生成。

Ozone-induced caspase-like activities are dependent on early ion channel regulations and ROS generation in Arabidopsis thaliana cells.

机构信息

Univ Paris Diderot, Sorbonne Paris Cité; Institut des Energies de Demain (IED, FRE 3597); Paris, France; Institut de Biologie des Plantes; Orsay, France.

出版信息

Plant Signal Behav. 2013 Aug;8(8). doi: 10.4161/psb.25170. Epub 2013 Jun 3.

DOI:10.4161/psb.25170
PMID:23733075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3999082/
Abstract

Using A. thaliana cultured cells; we recently reported new insights regarding the effect of acute O₃ exposure. This consist in an oxidative dependent controlled cell death process involving cell shrinkage due to an early activation of anion channel (1) and a delayed activation of K(+) outward currents, but also to early events like Ca (2+) influx or singlet oxygen production possibly linked to mitochondrial dysfunction. Here we provide evidence that most of these early events act downstream of caspase-like activities as recently demonstrated for K(+) channel activation.

摘要

我们最近使用拟南芥培养细胞报告了有关急性 O₃暴露影响的新见解。这涉及到一种依赖氧化的受控细胞死亡过程,该过程因阴离子通道的早期激活(1)和 K(+)外向电流的延迟激活而导致细胞收缩,但也涉及到 Ca(2+)内流或可能与线粒体功能障碍有关的单线态氧产生等早期事件。正如最近对 K(+)通道激活所证明的那样,这里我们提供的证据表明,这些早期事件中的大多数都作用于半胱天冬酶样活性的下游。