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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Elk-1 associates with the mitochondrial permeability transition pore complex in neurons
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Elk-1 associates with the mitochondrial permeability transition pore complex in neurons

机译：Elk-1与神经元中的线粒体通透性过渡孔复合物相关

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The nuclear transcription factor E-26-like protein 1 (Elk-1) is thought to impact neuronal differentiation [Sharrocks, A. D. (2001) Nat. Rev. Mol. Cell Biol. 2, 827-837], cell proliferation [Sharrocks, A. D. (2002) Biochem. Soc. Trans. 30,1-9], tumorigenesis [Chai, Y. L., Chipitsyna, G., Cui, J., Liao, B., Liu, S., Aysola, K., Yezdani, M., Reddy, E. S. P. & Rao, V. N. (2001) Oncogene 20, 1357-1367], and apoptosis [Shao, N., Chai, Y., Cui, J., Wang, N., Aysola, K., Reddy, E. S. P. & Rao, V. N. (11998) Oncogene 17, 527-532]. In addition to its nuclear localization, Elk-1 is found throughout the cytoplasm, including localization in neuronal dendrites [Sgambato, V., Vanhoutte, P., Pages, C., Rogard, M., Hipskind, R., Besson, M. J. & Caboche, J. (1998) J. Neurosci. 18, 214-226], raising the possibility that Elk-1 may have alternative extranuclear functions in neurons. Using coimmunoprecipitation and reciprocal coimmunoprecipitation from adult rat brain, we found an association between Elk-1 protein and the mitochondrial permeability transition pore complex (PTP), a structure involved in both apoptotic and necrotic cell death. Electron microscopy in adult rat brain sections confirmed this association with mitochondria. Elk-1 was also identified from purified mitochondrial fractions by using Western blotting, and Elk-1 increased its association with mitochondria following proapoptotic stimuli. Consistent with a role for Elk-1 in neuron viability, overexpression of Elk-1 in primary neurons decreased cell viability, whereas Elk-1 siRNA-mediated knockdown increased cell viability. This decrease in viability induced by Elk-1 overexpression was blocked with application of a PTP inhibitor. These results show an association of the nuclear transcription factor Elk-1 with the mitochondrial PTP and suggest an additional extranuclear function for Elk-1 in neurons.
机译：核转录因子E-26样蛋白1（Elk-1）被认为会影响神经元分化[Sharrocks，A.D。（2001）Nat.Natl.Acad.Sci.USA，87：1593-1877。牧师细胞生物学。 2，827-837]，细胞增殖[Sharrocks，A. D.（2002）Biochem。 Soc。反式30,1-9]，肿瘤发生[Chai，YL，Chipitsyna，G.，Cui，J.，Liao，B.，Liu，S.，Aysola，K.，Yezdani，M.，Reddy，ESP＆Rao，VN （2001）Oncogene 20，1357-1367]和凋亡[Shao，N.，Chai，Y.，Cui，J.，Wang，N.，Aysola，K.，Reddy，ESP＆Rao，VN（11998）Oncogene 17，527-532]。除其核定位外，在整个细胞质中还发现了Elk-1，包括在神经元树突中的定位[Sgambato，V.，Vanhoutte，P.，Pages，C.，Rogard，M.，Hipskind，R.，Besson，MJ ＆Caboche，J。（1998）J.Neurosci。 18，214-226]，增加了Elk-1在神经元中可能具有其他核外功能的可能性。使用成年大鼠大脑的免疫共沉淀和相互免疫共沉淀，我们发现Elk-1蛋白与线粒体通透性转换孔复合物（PTP）之间存在关联，该结构参与凋亡和坏死细胞死亡。成年大鼠脑切片的电子显微镜检查证实了这种与线粒体的联系。还使用Western印迹从纯化的线粒体级分中鉴定出Elk-1，并且在促凋亡后，Elk-1增加了其与线粒体的联系。与Elk-1在神经元生存能力中的作用一致，原代神经元中Elk-1的过表达降低细胞生存能力，而Elk-1 siRNA介导的敲低增加细胞生存能力。使用PTP抑制剂可阻止Elk-1过表达诱导的活力降低。这些结果表明核转录因子Elk-1与线粒体PTP之间存在关联，并提示神经元Elk-1具有额外的核外功能。

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