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首页> 外文期刊>Molecular biology of the cell >Cytotoxic necrotizing factor 1 prevents apoptosis via the Akt/I kappa B kinase pathway: Role of nuclear Factor-kappa B and Bcl-2
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Cytotoxic necrotizing factor 1 prevents apoptosis via the Akt/I kappa B kinase pathway: Role of nuclear Factor-kappa B and Bcl-2

机译：细胞毒性坏死因子1通过AKT / IκB激酶途径预防细胞凋亡：核因子-Kappa B和Bcl-2的作用

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摘要

Cytotoxic necrotizing factor 1 (CNF1) is a protein toxin produced by some pathogenic strains of Escherichia coli that specifically activates Rho, Rac, and Cdc42 GTPases. We previously reported that this toxin prevents the ultraviolet-B-induced apoptosis in epithelial cells, with a mechanism that remained to be defined. In this work, we show that the proteasomal degradation of the Rho GTPase is necessary to achieve cell death protection, because inhibition of Rho degradation abolishes the prosurvival activity of CNF1. We hypothesize that Rho inactivation allows the activity of Rac to become dominant. This in turn leads to stimulation of the phosphoinositide 3-kinase/Akt/I kappa B kinase/nuclear factor-kappa B prosurvival pathway and to a remarkable modification in the architecture of the mitochondrial network, mainly consisting in the appearance of elongated and interconnected mitochondria. Importantly, we found that Bcl-2 silencing reduces the ability of CNF1 to protect cells against apoptosis and that it also prevents the CNF1-induced mitochondrial changes. It is worth noting that the ability of a bacterial toxin to induce such a remodeling of the mitochondrial network is herein reported for the first time. The possible pathophysiological relevance of this finding is discussed.
机译：细胞毒性坏死因子1（CNF1）是由一定的大肠杆菌菌株产生的蛋白质毒素，其特异性激活Rho，RAC和CDC42 GTP酶。我们之前报道，该毒素可防止上皮细胞中紫外线-B诱导的细胞凋亡，其机制保持待定。在这项工作中，我们表明Rho GTP酶的蛋白酶体降解是实现细胞死亡保护所必需的，因为rho降解的抑制废除了CNF1的灭耐活性。我们假设Rho失活允许RAC的活动成为主导。这又导致磷酸阳性3-激酶/ AKT / IκBp激酶/核因子-Kappa刺激途径的刺激，并在线粒体网络的结构中具有显着的修饰，主要是组成的细长和相互连接的线粒体的外观。重要的是，我们发现Bcl-2沉默降低了CNF1保护细胞免受细胞凋亡的能力，并且它还可以防止CNF1诱导的线粒体变化。值得注意的是，本文首次报道了细菌毒素诱导线粒体网络这种重塑的能力。讨论了这种发现的可能的病理生理学相关性。

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