Necdin and TrkA contribute to modulation by p75NTR of resistance to oxidant stress

被引：8

作者：

Ingraham, Christopher A. ^{[1
]}

Schor, Nina F. ^{[1
]}

机构：

[1] Univ Rochester, Med Ctr, Dept Pediat, Rochester, NY 14642 USA

来源：

EXPERIMENTAL CELL RESEARCH | 2009年 / 315卷 / 20期

关键词：

p75NTR; Necdin; TrkA; Oxidant stress; Neurotrophin receptors; NGF; NERVE GROWTH-FACTOR; AFFINITY NGF RECEPTOR; PRADER-WILLI-SYNDROME; NEUROTROPHIN RECEPTOR; NEUROBLASTOMA-CELLS; MEDIATED APOPTOSIS; EXPRESSION; ACTIVATION; SURVIVAL; MOUSE;

D O I：

10.1016/j.yexcr.2009.10.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The neurotrophin receptor p75NTR provides protection from oxidant stress induced by 6-hydroxydopamine (6-OHDA) and resultant cell death. in the absence of p75NTR, TrkA is upregulated and its signaling pathway effectors are increasingly activated. Necdin, a MAGE protein and known interactor of p75NTR and TrkA, is a potential mediator of this phenomenon. Decreased expression of necdin protein in p75NTR-deficient PC12 cells decreased TrkA expression and increased PC12 cell resistance to 6-OHDA. Inhibition of JNK phosphorylation by SP600125 also resulted in increased resistance to 6-OHDA, suggesting that TrkA signaling underlies the susceptibility of these cells to oxidant stress. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：3532 / 3542

页数：11

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