The p75 receptor transduces the signal from myelin-associated glycoprotein to Rho.

The p75 receptor transduces the signal from myelin-associated glycoprotein to Rho.
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DOI:
10.1083/jcb.200202010
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发表时间:
2002-05-13
期刊:
The Journal of cell biology
影响因子:
--
通讯作者:
Tohyama M
Tohyama M
中科院分区:
其他
文献类型:
--
作者:
Yamashita T;Higuchi H;Tohyama M

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髓鞘相关糖蛋白(MAG)是一种有效的神经突生长抑制剂。MAG或引起神经元形态变化的信号的受体仍有待确定。本研究表明,神经营养因子受体p75 (p75NTR)是MAG的信号转导元件。携带p75NTR基因突变的小鼠的成年背根神经节神经元或出生后的小脑神经元在神经突生长方面对MAG不敏感。MAG激活小GTPase RhoA,当p75NTR存在时,导致生长迟缓。p75NTR和MAG结合的共定位在神经元中可见。神经节苷脂GT1b是MAG的结合伙伴之一,与p75NTR特异性结合。因此,p75NTR和GT1b可能形成MAG在神经元内传递抑制信号的受体复合物。
Myelin-associated glycoprotein (MAG) is a potent inhibitor of neurite outgrowth from a variety of neurons. The receptor for MAG or signals that elicit morphological changes in neurons remained to be established. Here we show that the neurotrophin receptor p75 (p75NTR) is the signal transducing element for MAG. Adult dorsal root ganglion neurons or postnatal cerebellar neurons from mice carrying a mutation in the p75NTR gene are insensitive to MAG with regard to neurite outgrowth. MAG activates small GTPase RhoA, leading to retarded outgrowth when p75NTR is present. Colocalization of p75NTR and MAG binding is seen in neurons. Ganglioside GT1b, which is one of the binding partners of MAG, specifically associates with p75NTR. Thus, p75NTR and GT1b may form a receptor complex for MAG to transmit the inhibitory signals in neurons.
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发表时间: 1997-01-01
影响因子: 3.5
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