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神经生长因子对顺铂神经毒性的挽救作用是通过高亲和力受体介导的:在PC12细胞和p75基因敲除小鼠背根神经节中的研究。

Nerve growth factor rescue of cisplatin neurotoxicity is mediated through the high affinity receptor: studies in PC12 cells and p75 null mouse dorsal root ganglia.

作者信息

Fischer S J, Podratz J L, Windebank A J

机构信息

Molecular Neuroscience Program, Mayo Graduate and Medical Schools, Rochester, MN 55905, USA.

出版信息

Neurosci Lett. 2001 Jul 27;308(1):1-4. doi: 10.1016/s0304-3940(01)01956-5.

DOI:10.1016/s0304-3940(01)01956-5
PMID:11445271
Abstract

Nerve growth factor (NGF) rescues dorsal root ganglion neurons and PC12 cells from cisplatin-induced cell death. Two model systems were used to demonstrate that rescue is mediated through the high affinity NGF receptor. In dorsal root ganglion (DRG) neurons isolated from p75(-/-) and control mice, 20 ng/ml NGF completely prevented cisplatin-induced death. In PC12 cells, we overexpressed receptor chimeras between the tumor necrosis factor and NGF receptors. We demonstrated that activation of the intracellular domain of Trk A is responsible for the NGF rescue effect.

摘要

神经生长因子(NGF)可挽救背根神经节神经元和PC12细胞免受顺铂诱导的细胞死亡。使用了两个模型系统来证明这种挽救作用是通过高亲和力NGF受体介导的。在从p75基因敲除小鼠和对照小鼠分离出的背根神经节(DRG)神经元中,20 ng/ml的NGF完全阻止了顺铂诱导的死亡。在PC12细胞中,我们过表达了肿瘤坏死因子受体和NGF受体之间的受体嵌合体。我们证明,Trk A细胞内结构域的激活是NGF挽救作用的原因。

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