TAJ/TROY, an orphan TNF receptor family member, binds Nogo-66 receptor 1 and regulates axonal regeneration

被引：321

作者：

Shao, ZH ^{[1
]}

Browning, JL ^{[1
]}

Lee, XH ^{[1
]}

Scott, ML ^{[1
]}

Shulga-Morskaya, S ^{[1
]}

Allaire, N ^{[1
]}

Thill, G ^{[1
]}

Levesque, M ^{[1
]}

Sah, D ^{[1
]}

McCoy, JM ^{[1
]}

Murray, B ^{[1
]}

Jung, V ^{[1
]}

Pepinsky, RB ^{[1
]}

Mi, S ^{[1
]}

机构：

[1] Biogen Inc, Dept Discovery Biol, Cambridge, MA 02142 USA

来源：

NEURON | 2005年 / 45卷 / 03期

关键词：

D O I：

10.1016/j.neuron.2004.12.050

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Myelin-associated inhibitory factors (MAIFs) are inhibitors of CNS axonal regeneration following injury. The Nogo receptor complex, composed of the Nogo66 receptor 1 (NgR1), neurotrophin p75 receptor (p75), and LINGO-1, represses axon regeneration upon binding to these myelin components. The limited expression of p75 to certain types of neurons and its temporal expression during development prompted speculation that other receptors are involved in the NgR1 complex. Here, we show that an orphan receptor in the TNF family called TAJ, broadly expressed in postnatal and adult neurons, binds to NgR1 and can replace p75 in the p75/NgR1/LINGO-1 complex to activate RhoA in the presence of myelin inhibitors. In vitro exogenously added TAJ reversed neurite outgrowth caused by MAIFs. Neurons from Taj-deficient mice were more resistant to the suppressive action of the myelin inhibitors. Given the limited expression of p75, the discovery of TAJ function is an important step for understanding the regulation of axonal regeneration.

引用

页码：353 / 359

页数：7

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